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Creative Touch Permanent Makeup and Aesthetics

Mitochondria

AnatomicalStructure Anatomical Structure

The common framing of mitochondria as “the powerhouse of the cell” understates their role in biology to the point of being misleading. In skin, mitochondria are simultaneously energy producers, quality control systems, developmental regulators, inflammatory triggers, and ageing rate determinants – with each function operating through a distinct mechanism that has direct consequences for how skin ages and how it responds to treatment. The most clinically significant of these functions is one that almost never appears in aesthetics content: mitochondria in produce not only as metabolic waste but as developmental signalling molecules that drive the differentiation programme that builds a functional . Understanding this dual role – ROS as damage and ROS as signal – reframes how antioxidant strategies are designed and timed in a treatment protocol. Alongside this, the mitochondrial genome (mtDNA) is the most UV-vulnerable DNA in the human body, accumulates damage at a rate measurably correlated with sun exposure history, and carries this damage in the dermal population most responsible for structural skin maintenance. Mitochondria are not a peripheral detail of skin cell biology – they are one of the core mechanistic axes around which , barrier function, and treatment response organise.

Structure and Basic Function

Mitochondria are double-membraned organelles of bacterial evolutionary origin – they retain their own genome (mtDNA), their own ribosomes, and their own replication machinery, all inherited from the ancestral proteobacterium that was engulfed by a eukaryotic precursor cell approximately 1.5 billion years ago. Each skin cell contains hundreds to thousands of mitochondria depending on cell type and metabolic demand – fibroblasts and keratinocytes in the are particularly mitochondria-rich, reflecting their high energy requirements for proliferation, synthesis, and differentiation. [6]

The primary function most familiar from general biology – ATP production – proceeds through (OXPHOS) in the inner mitochondrial membrane. The electron transport chain (ETC) comprises four enzyme complexes (I–IV) plus ATP synthase (Complex V), which collectively oxidise and FADH₂ from the citric acid cycle, transfer electrons to molecular oxygen, generate a proton gradient across the inner membrane, and use that gradient to drive ATP synthesis. The overall efficiency of this process is approximately 30–32 ATP molecules per glucose molecule – roughly 15 times the yield of anaerobic glycolysis. As discussed in the entity, when mitochondrial function declines in ageing keratinocytes, energy generation shifts toward glycolysis, producing what the Prahl et al. 2008 study characterised as “functionally anaerobic” skin – a metabolic state that reduces synthetic capacity and increases methylglyoxal-driven AGE formation simultaneously. [7] The clinical magnitude of this OXPHOS capacity decline as a determinant of biological age was quantified in the Baltimore Longitudinal Study of Ageing (2026): a 40-year-old with low mitochondrial oxidative capacity showed the same peak oxygen consumption as a 60-year-old of the same sex with high capacity – placing poor mitochondrial function at the heart of what distinguishes biological age from chronological age. [13]

The unavoidable by-product of ETC electron transfer is a proportion of electrons that escape the chain before reaching Complex IV and instead react with molecular oxygen to produce superoxide (O₂- ⁻) – the primary mitochondrial reactive oxygen species, converted by MnSOD to hydrogen peroxide (H₂O₂) and further to hydroxyl radical (- OH) via the Fenton reaction. MnSOD activity declines with age – epidermal Sod2 deficiency in mouse models produces the same accumulation of seen in naturally aged skin, confirming that declining mitochondrial antioxidant capacity is not merely a correlate of skin ageing but a driver of it. [14] Under normal conditions, approximately 1–2% of electrons that enter the ETC undergo this premature escape. Under conditions of ETC impairment – CoQ10 depletion, mtDNA damage, UV-induced Complex I dysfunction – this proportion increases substantially, producing the oxidative stress that characterises mitochondrially-driven ageing.

Mitochondrial Dynamics: Fusion, Fission, and Mitophagy

Mitochondria are not static structures – they exist in a continuous state of morphological flux, undergoing cycles of fusion (merging of adjacent mitochondria) and fission (division of a single mitochondrion into two daughter organelles), with damaged daughter mitochondria selectively cleared by mitophagy (autophagosomal engulfment and lysosomal degradation). [9] This fusion-fission-mitophagy cycle is a mitochondrial quality control system – arguably the most important endogenous mechanism by which cells maintain mitochondrial health across their lifespan.

Fusion is mediated by three GTPase proteins: Mitofusin 1 (MFN1) and Mitofusin 2 (MFN2) manage outer mitochondrial membrane fusion; OPA1 manages inner membrane fusion. Fusion allows adjacent mitochondria to share membrane lipid components, proteins, and mtDNA content – diluting localised mtDNA damage, redistributing functional ETC complexes to compensating underperforming neighbours, and temporarily restoring the mitochondrial network’s collective function. A fused, elongated mitochondrial network is the hallmark of a healthy, metabolically active cell. [9]

Fission is mediated by DRP1 (dynamin-related protein 1), recruited to outer membrane constriction sites by adaptor proteins FIS1 and MFF. Fission serves two complementary purposes: it generates smaller mitochondria that can be distributed to daughter cells during cell division, and it isolates severely damaged mitochondrial segments from the network – targeting them for mitophagy before their dysfunction propagates to neighbouring organelles. When fission is excessive relative to fusion – as occurs in UV-irradiated keratinocytes and aged fibroblasts – the result is a fragmented mitochondrial network of small, dysfunctional organelles that generate disproportionately high ROS and are cleared inefficiently, producing an accumulating deficit of functional mitochondrial capacity. [6]

The connection is precise here: stearic acid (C18:0) specifically stearoylates the transferrin receptor (TfR1), inhibiting JNK signalling and protecting MFN2 from HUWE1-mediated ubiquitination and proteasomal degradation – preserving MFN2 protein levels and sustaining the fusion arm of the dynamic balance. (C16:0) does not produce this response, despite being structurally adjacent. The consequence is a more interconnected, functionally efficient mitochondrial network in cells with adequate stearic acid – and why the stearic acid entity’s mitochondrial fusion finding belongs in a mechanistic cross-reference here, not as an isolated curiosity. [9]

Clinical Pearl: UV exposure in keratinocytes specifically activates DRP1-dependent fission – depletion of DRP1 in UV-irradiated keratinocytes significantly attenuates both fragmentation and the downstream ROS burst that follows it. DRP1 is therefore a mechanistic target for UV-protective strategies beyond simple antioxidant approaches. [6]

The mtDNA Common Deletion: Photoageing’s Molecular Fingerprint

Mitochondrial DNA is the most UV-vulnerable nucleic acid in human skin for three structural reasons: it is not protected by histones (unlike nuclear DNA), it has limited excision repair capacity compared to the nuclear DNA damage response system, and it is physically located adjacent to the inner mitochondrial membrane – the primary intracellular ROS generation site. [8] This proximity means that every burst of ETC-derived ROS exposes the mitochondrial genome to oxidative attack from nanometre distances.

The most studied consequence of cumulative mtDNA damage in skin is the 4977 base pair (bp) common deletion – a deletion that removes a 4,977 bp segment spanning the region between two direct repeat sequences in the mitochondrial genome. This segment encodes subunits of ETC Complexes I, III, IV, and V – the core respiratory machinery. A mitochondrion carrying the common deletion cannot assemble functional versions of these complexes and is metabolically impaired regardless of substrate availability. [1] Critically, the deletion is not repaired – it accumulates through successive cell divisions and clonal expansion, producing an increasing proportion of deletion-carrying mtDNA molecules in affected cells over time.

The quantification of the common deletion is among the most striking in skin biology research: dermal fibroblasts from photodamaged skin carry 6.9 times more common deletion than those from sun-protected skin of the same individual – measured from paired biopsies of sun-exposed dorsal forearm versus sun-protected upper inner arm in the same donors. Chronological ageing alone – comparing young versus aged sun-protected skin – produces a 4.5-fold increase, confirming that UV exposure compounds the age-related deletion accumulation substantially beyond what time alone produces. [8] This deletion accumulates predominantly in the rather than the – directly in the fibroblast population responsible for I, collagen III, and synthesis.

Fontana et al. (2026) provide the mechanistic distinction between UVA and UVB contributions to common deletion formation: UVA induces the common deletion via a ROS-dependent mechanism – antioxidant pre-treatment prevented UVA-induced deletion formation – whilst UVB induces it through a ROS-independent mechanism via cyclobutane pyrimidine dimer (CPD) formation in the mtDNA itself. This mechanistic split has direct practical implications: topical antioxidants in sunscreen formulations address UVA-driven mtDNA damage through the ROS pathway, whilst SPF’s UVB absorption addresses a structurally distinct mechanism that antioxidants alone cannot prevent. Both strategies are needed for comprehensive mtDNA protection – they are not interchangeable. [2]

Mitochondria as Keratinocyte Differentiation Gatekeepers

One of the most counterintuitive and clinically important findings in skin mitochondrial biology is that mitochondrial ROS are not simply damaging waste products in keratinocytes – at physiological levels, they are required signalling molecules that drive the commitment to . [4]

The evidence comes from the TFAM conditional knockout model (Hamanaka et al., 2013). TFAM (mitochondrial transcription factor A) is required for mtDNA replication and transcription – TFAM-deleted keratinocytes cannot conduct oxidative phosphorylation or produce mitochondrial ROS. The predicted outcome was impaired keratinocyte viability or barrier function. The actual outcome was profoundly disrupted epidermal stratification: the differentiation programme that drives keratinocytes from the basal layer through the spinous, granular, and cornified layers failed to execute normally, producing an epidermal architecture that could not form a properly organised stratum corneum. cycling was severely disrupted concurrently. [4]

Critically, when wild-type keratinocytes were treated with exogenous antioxidants to suppress mROS, differentiation was similarly impaired – and when TFAM-deleted keratinocytes were exposed to exogenous H₂O₂ at physiological levels, differentiation markers were partially restored. The mitochondrial ROS signal – at physiological concentrations – is a necessary biochemical input to the differentiation pathway. The downstream mechanism involves mROS activation of the Notch and AP-1 pathways, which control the transcription factor cascades driving differentiation commitment. [4]

This finding does not argue against antioxidant use in skincare – physiological mROS signalling occurs intracellularly, and topically applied antioxidants at cosmetic concentrations are unlikely to significantly suppress this signal in the basal keratinocyte layer. However, it establishes an important conceptual boundary: mitochondrial ROS in skin are a dual-function molecule, and the goal of mitochondrial protection is not ROS elimination but ROS calibration – reducing pathological excess whilst preserving the physiological signal.

Fibroblast Senescence: The Mechanical Tension → ROS → mtDNA Loop

The Quan et al. 2015 study identified a mechanistic loop in dermal fibroblast ageing that connects ECM loss directly to mitochondrial dysfunction through a physical rather than purely biochemical pathway. [8]

As dermal ECM volume declines with age – through reduced synthesis, increased MMP degradation, and ground substance depletion – dermal fibroblasts lose the mechanical tension of their surrounding matrix. Fibroblast cell spreading area (the physical extent to which a fibroblast flattens and extends across its substrate, dependent on matrix mechanical resistance) decreases. Reduced cell spreading in fibroblasts directly increases mitochondrial ROS production – through a mechanosensing mechanism involving cytoskeletal tension loss and subsequent alteration of mitochondrial membrane potential. The elevated ROS then induce the mtDNA common deletion in those fibroblasts, impairing their ETC function and generating more ROS in a self-amplifying loop. [8]

The loop runs: ECM loss → reduced fibroblast spreading → elevated mROS → mtDNA common deletion accumulation → ETC impairment → more mROS → more deletion. Breaking the loop at the ECM mechanical tension step – by restoring matrix volume and fibroblast cell spreading – reduces the endogenous mROS burden and slows deletion accumulation. Quan et al. explicitly make this connection within the paper itself, citing their own 2007 in vivo dermal filler study (Wang et al.): injection of cross-linked into the skin of individuals over 70 years of age enhanced fibroblast cell spreading, stimulated collagen production and proliferation, expanded vasculature, and increased epidermal thickness – confirming that restoring mechanical tension in aged dermis reverses the collapsed fibroblast phenotype in living tissue, not only in culture models. [8] This gives the HA skin booster’s mechanical tension restoration mechanism an additional dimension not covered in the HA entity: beyond activation and procollagen stimulation, HA-restored matrix tension is also a mitochondrial protection strategy – one with in vivo human evidence – reducing the ROS burden that drives the common deletion accumulation responsible for progressive fibroblast dysfunction.

Inflammation: cGAS-STING and the Innate Immune Activation

When mitochondrial integrity is sufficiently compromised – by UV damage, sustained ROS excess, ageing-related membrane permeabilisation, or acute cellular injury – damaged mtDNA fragments and whole mitochondria or their debris can escape into the cytosol. [3] The innate immune system is constitutively primed to detect cytosolic DNA as a danger signal – the presence of DNA outside the nucleus or mitochondria indicates cell damage or pathogen invasion – and two pathways respond to cytosolic mtDNA in skin cells:

The cGAS-STING pathway: Cyclic GMP- synthase (cGAS) detects cytosolic double-stranded DNA, generates the second messenger cGAMP, which activates STING (stimulator of interferon genes), triggering activation and a pro-inflammatory cytokine cascade – , IL-1β, , and type I interferons. [3]

In dermal fibroblasts specifically, the cGAS-STING cascade can be triggered by a metabolic route distinct from UV damage: suppression of carnitine acetyltransferase (CRAT) – a key enzyme supplying acetyl groups for OXPHOS – causes mitochondrial dysfunction, cytosolic mtDNA release, and activation of the full cGAS-STING → NF-κB → inflammatory cascade. [12] This metabolic pathway connects the fibroblast’s energy state directly to its inflammatory output, independently of UV exposure or exogenous damage.

The NLRP3 inflammasome: Mitochondrial ROS and mtDNA fragments activate the NLRP3 inflammasome in keratinocytes and dermal macrophages, producing mature IL-1β and IL-18 via caspase-1 cleavage.

This mtDNA-to-inflammation axis is the molecular basis of in skin – the chronic, low-grade, sterile inflammation that drives progressive structural deterioration in the absence of infection or acute injury. It is distinct from the cytokine-mediated inflammation targeted by or (which address / and NF-κB respectively), establishing mitochondrial health as an independent anti-inflammatory target – one that upstream interventions protecting mtDNA integrity (antioxidants, fusion preservation) address at the source rather than the cytokine output level. [5]

Melanogenesis: The Fission-MITF-Pigmentation Axis

Mitochondrial fission in and their precursors activates the ROS-ERK signalling pathway, which phosphorylates and drives proteasomal degradation of (microphthalmia-associated transcription factor) – the master transcriptional regulator of melanocyte differentiation and melanin synthesis gene expression. [6] When MITF levels fall through fission-driven ERK activation, melanin synthesis is reduced – tyrosinase, TRP-1, and TRP-2 are all MITF target genes.

This pathway has two clinically relevant implications. First, the melanocytic stem cells (McSCs) in the hair follicle bulge – already discussed in the entity – are sensitive to mitochondrial dysfunction in ways that accelerate their depletion through successive hair cycles, contributing to the melanocytic stem cell exhaustion that drives hair greying. Second, post-procedure and post-inflammatory pigmentation inconsistency may be partially attributable to mitochondrial disruption in perifollicular and epidermal melanocytes following thermal or physical treatment – a mechanism distinct from the TYR-upregulation pathway of conventional post-inflammatory and potentially responsive to different mitochondrial-targeted approaches.

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Clinical Application

Mitochondrial health in skin does not map neatly onto either category of the established treatment framework – it is not purely a direct synthesis stimulation, or an inflammatory barrier removal target. It is better understood as the upstream substrate layer that determines how effectively both categories perform: direct synthesis treatments stimulate fibroblasts and keratinocytes whose synthetic output is ultimately constrained by their mitochondrial energy capacity; inflammatory barrier removal treatments reduce the cytokine burden that suppresses synthesis, but cannot restore the ETC function that progressive mtDNA deletion has impaired. Mitochondrial restoration is the third axis – the one that determines how much capacity is available to be activated by everything else. [3]

The practical clinical implication is a diagnostic one: a client who under-responds to treatments that should produce measurable improvement – collagen stimulation protocols, barrier repair programmes, hair follicle cycling interventions – warrants assessment of the mitochondrial health factors in their history: cumulative UV exposure, statin use, dietary and NAD⁺ precursor intake, and the quality of their antioxidant and photoprotection habits. Mitochondrially compromised dermis has impaired fibroblast synthetic capacity that no amount of TGF-β signalling will fully overcome whilst the underlying ETC deficit persists.

Red LED: The Only Direct ETC Intervention in the Portfolio

in the 630–660nm wavelength range is the sole treatment in the Creative Touch portfolio that directly interfaces with the mitochondrial electron transport chain. According to the leading mechanistic hypothesis, its primary photoacceptor is cytochrome c oxidase – the copper and haem-containing enzyme of Complex IV that accepts electrons from cytochrome c and transfers them to molecular oxygen, completing the ETC. [3] Within this model, red light photons are absorbed by the copper centres within cytochrome c oxidase, dissociating inhibitory nitric oxide (NO) bound to the enzyme’s active site – NO competitively inhibits oxygen binding at Complex IV and is a significant contributor to the mitochondrial respiratory impairment in UV-damaged and aged skin. Removal of this inhibition restores electron transfer rate, improves the proton gradient, and increases ATP synthesis.

The downstream consequences extend beyond simple energy restoration: improved ETC efficiency reduces the proportion of electrons escaping as superoxide, directly lowering the endogenous ROS burden that drives both mtDNA common deletion accumulation and the cGAS-STING inflammatory cascade. Red LED is therefore simultaneously an energy intervention, an antioxidant intervention, and an anti-inflammatory intervention – all mediated through the same cytochrome c oxidase photodissociation mechanism.

Positioning: Red LED as a post-procedure adjunct following , FTL, or chemical peel provides mitochondrial support during the highest-demand phase of the repair cycle – when keratinocytes are actively proliferating for re-epithelialisation and fibroblasts are maximally activated for ECM synthesis. Both processes are energy-intensive; restoring mitochondrial respiratory efficiency at this precise phase maximises the capacity of the cell populations doing the repair work.

CoQ10 and Niacinamide: Substrate Restoration

Where red LED acts on the ETC machinery directly, CoQ10 and act on the substrate availability that the machinery requires.

Topical CoQ10 restores the mobile electron carrier depleted by UV exposure and age-related decline, directly supporting Complex I–III electron transfer. As established in the CoQ10 entity, topical application confirms penetration to viable epidermal layers and measurable metabolic conversion – the reversal of the “functionally anaerobic” keratinocyte metabolic shift observed by Prahl et al. is the most clinically legible outcome of this restoration. [7] For clients on statin therapy – where HMG-CoA reductase inhibition co-depletes CoQ10 and through the shared mevalonate pathway – topical CoQ10 provides mitochondrial substrate restoration that oral supplementation does not reliably deliver to skin specifically.

Niacinamide connects to mitochondrial function through the NAD⁺ pathway. Niacinamide → NAD⁺ conversion provides the substrate for SIRT3 (a mitochondria-localised deacylase) that deacetylates and activates Complex I subunits, improving ETC efficiency, and for SIRT1, which activates PGC-1α – the master regulator of mitochondrial biogenesis that drives production of new functional mitochondria to replace those cleared by mitophagy. Niacinamide’s synthesis and barrier repair benefits, well-established in the Niacinamide entity, are therefore accompanied by a parallel mitochondrial maintenance mechanism that is rarely cited in the clinical rationale for its use.

Treatment pairing – CoQ10 + Niacinamide: Acting on two distinct mitochondrial substrate pathways simultaneously – electron carrier availability (CoQ10) and NAD⁺-dependent ETC activation and biogenesis (niacinamide) – this combination addresses mitochondrial function more completely than either alone. Both are compatible, non-competing actives formulated into serums at therapeutic concentrations, making the combination a practical homecare recommendation for clients with identified mitochondrial risk factors.

Stearic Acid: Preserving the Fusion Balance

The MFN2 stearoylation mechanism described in the Stearic Acid entity is directly applicable here as a fusion preservation strategy. Stearic acid (C18:0) – found in cocoa butter, , , and dairy fat – specifically stearoylates TfR1, inhibiting JNK signalling and protecting MFN2 from HUWE1-mediated ubiquitination, maintaining the fusion arm of the mitochondrial dynamic balance. [10] Human confirmation that dietary C18:0 ingestion causes mitochondrial fusion within three hours – whilst the equivalent C16:0 dose produces no response – is established in Senyilmaz-Tiebe et al. 2018. [11] In the context of the fission-predominant mitochondrial fragmentation that characterises UV-damaged and aged skin, dietary stearic acid adequacy becomes a meaningful nutritional variable – not in the supplementation sense, but in the dietary pattern sense. Clients with very low saturated fat intake may be inadvertently compromising the fusion-preservation mechanism that maintains mitochondrial network integrity.

This is a client conversation point rather than a treatment recommendation: it belongs in the nutritional context discussion alongside intake, not as a prescription or protocol step.

HA Skin Boosters: Mechanical Tension and the ROS Loop

The Quan et al. 2015 finding – that injection of cross-linked hyaluronic acid into aged skin restores fibroblast cell spreading, reduces mROS generation, and slows mtDNA common deletion accumulation – establishes HA as a mitochondrial protection intervention through a physical rather than biochemical mechanism. [8] The clinical framing most clients receive for skin boosters – “hydration and collagen stimulation” – is accurate but incomplete. Restoring matrix mechanical tension is simultaneously restoring the cell-spreading conditions under which dermal fibroblasts produce less endogenous ROS, accumulate the common deletion more slowly, and preserve ETC function for longer.

For clients with significant photoageing and dermal volume loss – where the reduced-spreading → ROS → deletion loop is already well-established – the mitochondrial protective rationale for a mid-dermal HA booster programme is as mechanistically sound as the TGF-β collagen stimulation rationale, and the two are inseparable in practice.

Treatment pairing – HA booster + polynucleotides: HA restores mechanical tension, reducing the endogenous mROS burden that drives common deletion accumulation. Polynucleotides suppress NF-κB, reducing the exogenous inflammatory cytokine burden that compounds the mtDNA-driven cGAS-STING inflammatory cascade. The two treatments address the mitochondrial ageing loop at different entry points – physical (mechanical tension) and biochemical (cytokine suppression) – producing a more complete mitochondrial protection environment than either delivers alone. This pairing logic is consistent with the Category B treatment framework and adds a mitochondrial protection dimension to the combination rationale already established in the Collagen and Elastin clinical contexts.

Antioxidant SPF: The Dual-Mechanism mtDNA Protection Strategy

The 2026 UVA/UVB mechanistic distinction – UVA induces the common deletion via ROS-dependent pathway; UVB via ROS-independent CPD formation – has a direct practical consequence for daily photoprotection advice. A sunscreen that blocks UVB but contains no antioxidant component addresses the CPD-driven UVB mechanism but leaves the UVA ROS-driven mechanism unprotected. An antioxidant-containing formulation without adequate UVA blocking addresses neither adequately. Complete mtDNA protection requires both: [2]

  • Broad-spectrum SPF (UVA + UVB): Physical or chemical UV absorption preventing both CPD formation (UVB) and the ROS-generating photochemical reactions (UVA) from reaching dermal fibroblasts
  • Topical antioxidants ( , , CoQ10) in the underlying serum layer: Scavenging the ROS that penetrate despite UV filtering, specifically interrupting the UVA → ROS → common deletion pathway

Vitamin C’s dual function – aqueous-phase ROS scavenging and -1 suppression – makes it the most mechanistically complete antioxidant for this layered protection. The combination of a vitamin C serum under an SPF 30+ broad-spectrum sunscreen is not a routine marketing recommendation but a mechanistically complete anti-photoageing protocol that addresses mtDNA protection through both available pathways simultaneously.

The mROS Paradox: Why Antioxidant Loading Has Limits

The TFAM conditional knockout finding – that physiological mitochondrial ROS are required signals for keratinocyte differentiation commitment – establishes an important clinical boundary. [4] The goal of mitochondrial antioxidant strategy is not ROS elimination but ROS calibration: reducing the pathological excess generated by ETC impairment and UV damage, whilst preserving the physiological intracellular signal that drives the differentiation programme responsible for building a functional stratum corneum.

In practical terms, this boundary is unlikely to be breached by standard topical antioxidant application – physiological mROS signalling occurs intracellularly within the basal keratinocyte layer, and cosmetically applied antioxidants at standard formulation concentrations are not expected to meaningfully suppress this intracellular signal. However, it is relevant in two specific contexts:

  • Very high-concentration antioxidant cocktails applied immediately post-procedure: Treatments that intentionally generate controlled ROS signals – RF microneedling, , – depend on those signals for part of their wound-healing activation mechanism. Applying very high-concentration antioxidant formulations within the first hour post-treatment may theoretically blunt this signal. The practical recommendation remains to apply antioxidant-rich formulations after the initial acute ROS-signalling window (24–48 hours post-procedure) rather than immediately. Post-procedure , ceramide repair, and red LED are appropriate immediate post-procedure interventions; high-dose antioxidant serum belongs in the day three onwards recovery phase.

  • Client counselling on oral antioxidant supplementation: Extremely high-dose oral antioxidant supplementation has produced counter-productive results in exercise physiology (blunting mitochondrial adaptation to exercise training). Whilst not a current evidence concern in the dermatology context, it supports a calibrated rather than maximum-dose approach to antioxidant supplementation advice.

References

  1. Birch-Machin MA, Tindall M, Turner R, et al. (1998). Mitochondrial DNA deletions in human skin reflect photo- rather than chronologic aging. J Invest Dermatol, 110(2), 149-52 .

  2. Fontana Gabriele A., Singh Navnit K., Rotankova Nadezhda, et al. (2026). UVA Irradiation Promotes ROS-Mediated Formation of the Common Deletion in Mitochondrial DNA. Life, 16(4), 577 .

  3. Golubnitschaja O, Sargheini N, Bastert J (2025). Mitochondria in cutaneous health, disease, ageing and rejuvenation-the 3PM-guided mitochondria-centric dermatology. EPMA J, 16(1), 1-15 .

  4. Hamanaka RB, Chandel NS (2013). Mitochondrial metabolism as a regulator of keratinocyte differentiation. Cell Logist, 3(1), e25456 .

  5. Li C, Zhu Y, Liu W, et al. (2023). Increased mitochondrial fission induces NLRP3/cGAS-STING mediated pro-inflammatory pathways and apoptosis in UVB-irradiated immortalized human keratinocyte HaCaT cells. Arch Biochem Biophys, 738, 109558 .

  6. Martic I, Papaccio F, Bellei B, et al. (2023). Mitochondrial dynamics and metabolism across skin cells: implications for skin homeostasis and aging. Front Physiol, 14, 1284410 .

  7. Prahl S, Kueper T, Biernoth T, et al. (2008). Aging skin is functionally anaerobic: importance of coenzyme Q10 for anti aging skin care. Biofactors, 32(1-4), 245-55 .

  8. Quan C, Cho MK, Perry D, et al. (2015). Age-associated reduction of cell spreading induces mitochondrial DNA common deletion by oxidative stress in human skin dermal fibroblasts: implication for human skin connective tissue aging. J Biomed Sci, 22(1), 62 .

  9. Quan T, Li R, Gao T (2025). Role of Mitochondrial Dynamics in Skin Homeostasis: An Update. Int J Mol Sci, 26(5) .

  10. Senyilmaz D, Virtue S, Xu X, et al. (2015). Regulation of mitochondrial morphology and function by stearoylation of TFR1. Nature, 525(7567), 124-8 .

  11. Senyilmaz-Tiebe D, Pfaff DH, Virtue S, et al. (2018). Dietary stearic acid regulates mitochondria in vivo in humans. Nat Commun, 9(1), 3129 .

  12. Song MJ, Park CH, Kim H, et al. (2023). Carnitine acetyltransferase deficiency mediates mitochondrial dysfunction-induced cellular senescence in dermal fibroblasts. Aging Cell, 22(11), e14000 .

  13. Trevisan C, Tian Q, Fishbein KW, et al. (2026). Association of mitochondrial oxidative capacity with physical fitness in ageing: the Baltimore longitudinal study of ageing. Age Ageing, 55(2) .

  14. Velarde MC, Flynn JM, Day NU, et al. (2012). Mitochondrial oxidative stress caused by Sod2 deficiency promotes cellular senescence and aging phenotypes in the skin. Aging (Albany NY), 4(1), 3-12 .

Also Known As

  • mitochondrion

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  • Affects Cellular senescence
  • Affects Inflammageing
  • Affects Skin ageing
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  • Related therapy

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