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Melanocyte

AnatomicalStructure Cell Type

Melanocytes are the pigment-producing cells of the , responsible for synthesising melanin and transferring it to surrounding in response to UV exposure. Their function extends beyond pigmentation: the keratinocyte–melanocyte signalling axis mediates UV-induced DNA repair in keratinocytes through a pigmentation-independent pathway, making melanocyte activity a broader component of epidermal UV defence than its cosmetic role implies. With ageing, melanocyte density declines at approximately 10–20% per decade in sun-protected . More significantly, melanocytes are the only epidermal cell type to express the senescence marker p16INK4A under normal ageing conditions, and senescent melanocytes drive epidermal atrophy through paracrine telomere damage in surrounding keratinocytes, positioning them as active contributors to rather than passive bystanders of it.

Melanocytes are specialised dendritic cells located in the of the epidermis, derived embryologically from neural crest cells that migrate to the skin during foetal development. They constitute approximately 5–10% of basal epidermal cells, distributed at a density of roughly one melanocyte per 35–40 keratinocytes – a ratio maintained with remarkable consistency across different skin phototypes despite wide variation in the melanin output per cell. Their primary function is the synthesis of melanin within organelles called melanosomes, which are then transferred to surrounding keratinocytes via dendritic projections. Each melanocyte serves approximately 36 keratinocytes in this way, forming the epidermal melanin unit – a functional pairing that underpins the skin’s primary photoprotective system. [4]

Melanin Synthesis and the UV Response

Melanin production is not a constitutive background process but dynamically regulated by a well-characterised paracrine signalling axis between keratinocytes and melanocytes. UV irradiation activates p53 in keratinocytes, which upregulates expression of the POMC gene and triggers release of alpha-melanocyte-stimulating hormone (α-MSH). α-MSH binds to melanocortin-1 receptor (MC1R) on melanocyte surfaces, activating adenylate cyclase and elevating intracellular . This cAMP signal activates MITF – the master transcription factor governing melanocyte identity and function – which upregulates the enzymatic machinery of melanin synthesis, shifting output toward eumelanin, the brown-black photoprotective form over phaeomelanin, the red-yellow form with lower photoprotective capacity. [4]

What is less widely appreciated is that this signalling axis also directly enhances DNA repair in keratinocytes through a pathway independent of pigmentation entirely. α-MSH binding to MC1R in keratinocytes activates adenylate cyclase, which in turn promotes nuclear translocation of XPA – a rate-limiting factor in nucleotide excision repair (NER), the primary pathway for removing UV-induced DNA photoproducts. This means that impaired MC1R signalling – through MC1R loss-of-function variants common in fair-skinned, red-haired individuals – reduces not only pigmentation but also the DNA repair capacity of the epidermis, directly increasing UV mutagenic risk. [3]

The MC1R Receptor

MC1R is the G-protein-coupled receptor through which α-MSH exerts its pigmentary and non-pigmentary effects in the skin. Its activation by α-MSH triggers adenylyl cyclase-mediated cAMP production, initiating the PKA signalling cascade that activates MITF and shifts melanin synthesis toward eumelanin. The receptor is expressed not only on melanocytes but on keratinocytes and immune cells, where the same cAMP signal suppresses activation – making MC1R a convergence point between the pigmentation and cutaneous immune-suppression arms of the UV response.

MC1R loss-of-function variants – particularly R151C, R160W, and D294H, collectively designated the RHC (red hair colour) alleles – are among the most clinically significant common polymorphisms in skin biology. Carriers of a single MC1R variant carry approximately 40% increased melanoma risk; carriers of two or more variants carry more than double the risk of wild-type subjects, and this association holds independently of UV exposure, skin phototype, and tanning behaviour. [10] [13] The elevated risk operates through two concurrent mechanisms: reduced eumelanin photoprotection and – as described in the UV response section above – impaired MC1R-dependent XPA nuclear translocation and nucleotide excision repair in keratinocytes.

In the context of energy-based and laser treatments, MC1R variant status is a meaningful pre-treatment risk factor that sits beneath the commonly used Fitzpatrick skin type classification. A fair-skinned Fitzpatrick I–II client with known RHC variants carries a biologically distinct UV sensitivity and post-inflammatory response profile from a phenotypically similar client with wild-type MC1R, with implications for post-treatment risk, healing trajectory, and long-term skin cancer surveillance.

Alpha-MSH and the Cutaneous Stress Response

Alpha-melanocyte-stimulating hormone (α-MSH) is the primary melanogenic and anti-inflammatory released from in the skin, and its function extends well beyond pigmentation. As described in the UV response section, the UV→p53→POMC→α-MSH axis is the best-characterised route to MC1R activation – but it operates in parallel with a second, independently regulated pathway. Psychological and physiological stress activates the cutaneous CRH/POMC system through (CRH) released locally within the skin, producing POMC-derived peptides including α-MSH and ACTH without requiring UV exposure. [16] The same downstream signal – cAMP elevation, MITF activation, eumelanin upregulation – is reached by either route, which is why stress-associated pigmentation changes and UV-induced tanning share a common effector mechanism despite different initiating signals.

The anti-inflammatory dimension of α-MSH is distinct from its pigmentary role and operates in parallel with it. By suppressing NF-κB activation in keratinocytes and immune cells, α-MSH acts as a physiological brake on the pro-inflammatory cytokine cascade that follows UV irradiation. This positions the POMC→α-MSH pathway not merely as a tanning signal but as a coordinated damage-response system – driving both photoprotective pigmentation and local immune modulation simultaneously from the same molecular event. Chronic stress, paradoxically, suppresses cutaneous POMC expression through glucocorticoid-dependent negative feedback, reducing both the pigmentary and immunomodulatory outputs of the axis at a time of elevated systemic inflammatory load. [12]

MITF: The Melanocyte Master Regulator

Microphthalmia-associated transcription factor (MITF) functions as the master transcriptional regulator of melanocyte identity – governing not only the enzymatic machinery of melanin synthesis (TYR, TYRP1, DCT) but also melanocyte differentiation, survival, and cell cycle progression. It is the terminal effector of the α-MSH→MC1R→cAMP→PKA signalling axis and the point at which the upstream stress and UV signals are converted into coordinated changes in melanocyte gene expression. MITF is not a dedicated pigmentation switch but a broad lineage regulator: its activity level determines whether a melanocyte proliferates, differentiates, or undergoes apoptosis, rather than simply whether it is active or inactive. [9]

This regulatory centrality makes MITF a significant factor in melanoma biology. MITF is amplified in approximately 30–40% of melanomas, where it functions as a lineage addiction oncogene – driving proliferation in a cell type in which it is already constitutively expressed at high levels. [14] Its role is not straightforwardly oncogenic: MITF activity level appears to determine melanoma cell phenotype along a proliferative–invasive axis, with high MITF expression associated with proliferative, differentiated tumour cells and low MITF expression associated with invasive, dedifferentiated behaviour. [7] This phenotypic switching model has implications for understanding melanoma progression and treatment resistance, and it explains why MITF status in melanoma is not a simple binary risk marker.

Melanocytes in Skin Ageing

Melanocyte density in sun-protected skin declines at approximately 10–20% per decade from the third decade onward – a gradual attrition that contributes to uneven pigmentation, reduced tanning response capacity, and diminished UV defence over time. In photoaged skin this decline is accompanied by focal areas of melanocyte hyperactivity, producing the dyspigmentation and irregular distribution characteristic of UV-accumulated skin.

The more significant ageing finding concerns senescence. A 2019 study published in the EMBO Journal established that melanocytes are the only epidermal cell type to express p16INK4A – the canonical marker of – under normal human ageing conditions. Senescent melanocytes do not merely stop functioning; they actively impair surrounding keratinocyte proliferation through paracrine telomere damage, inducing p16INK4A expression in keratinocytes and reducing their replicative capacity. The consequence in three-dimensional epidermal models was measurably thinner epidermis with fewer keratinocyte layers and reduced -10 expression, markers of the epidermal atrophy characteristic of aged skin. Clearance of senescent melanocytes using senolytic intervention reversed these effects, confirming causation rather than correlation. [18]

This positions melanocyte senescence as a meaningful independent driver of epidermal ageing, one that operates through -like paracrine signalling on the same keratinocyte population that maintains barrier function and epidermal thickness. It is a mechanism that sits alongside the senescence and ground substance depletion stories established in the , and it deserves the same clinical attention.

Melanocyte Stem Cells and Hair Greying

Melanocytes in are replenished each hair growth cycle from a melanocyte stem cell (McSC) population residing in the hair follicle bulge. These stem cells must traffic between the bulge and the hair germ compartment, differentiating in the hair germ to produce melanocytes for the new hair, then returning to the bulge to maintain their stem cell state. With repeated hair cycles and advancing age, increasing numbers of McSCs become trapped between the two compartments, unable to complete either differentiation or self-renewal. This trafficking failure depletes the McSC pool faster than any other adult stem cell population, producing the greying that precedes hair follicle structural decline. [17] Notably, McSC depletion occurs substantially earlier than hair follicle stem cell depletion – the pigmentation system is more fragile than the hair growth system it serves.

The Cutaneous HPA Axis and POMC

The skin expresses a complete functional homologue of the hypothalamic-pituitary-adrenal () axis, operating as a localised stress-response system independent of – though capable of communicating with – the central HPA axis. This cutaneous HPA axis includes local expression of CRH, POMC, and the downstream receptors for their cleavage products, enabling the skin to generate , α-MSH, and β-endorphin in situ in response to UV irradiation, physical injury, or stress signals. [15] The biological function of this local system is integrative – simultaneously coordinating photoprotective pigmentation (via α-MSH→MC1R→MITF), local synthesis (via ACTH→MC2R), anti-inflammatory signalling (via α-MSH NF-κB suppression), and pain and itch modulation (via β-endorphin→opioid receptors) within the same tissue under the same stimulus.

The UV wavelength-dependence of cutaneous POMC activation is clinically relevant. UVB and UVC are the primary activating stimuli for the cutaneous HPA axis, operating through the UV→p53→POMC pathway in keratinocytes; UVA activates overlapping but partially distinct mechanisms. [15] This wavelength specificity means that broad-spectrum UV exposure from natural sunlight engages the full cutaneous POMC system in a way that filtered or narrowband light sources may not replicate – a distinction relevant to phototherapy protocols and to understanding the limits of artificial UV modalities as substitutes for natural sun exposure in research contexts.

Melanocyte Ageing: Density Decline and Focal Clustering

Cutaneous ageing presents a paradox at the level of the melanocyte population: overall cell density declines progressively with chronological age, yet photodamaged skin simultaneously displays focal zones of markedly increased pigmentation. Understanding why these two phenomena coexist – rather than counteracting one another – requires distinguishing between the fate of the bulk melanocyte population and the behaviour of the cells that survive.

The density decline

From approximately the third decade of life, the number of enzymatically active melanocytes – identifiable by the DOPA reaction – decreases at a rate of roughly 6–20% per decade depending on anatomical site, cumulative ultraviolet (UV) exposure, and the counting method applied [5]. The widely cited figure of “10–20% per decade” derives from a 1990 synthesis of multiple studies [11] and reflects greater variance across sites and UV exposure histories. In habitually sun-exposed skin, melanocyte density is approximately twice that of unexposed skin at equivalent ages [5], indicating that UV irradiation stimulates melanocyte survival or proliferation whilst simultaneously accelerating the longer-term attrition of the population.

This loss is not uniform. Where melanocytes are depleted, the resulting areas of relative hypomelanosis produce the generalised even-tone loss and pallor associated with intrinsically aged or photoprotected skin. In sun-exposed skin, by contrast, the picture is more complex.

The activation paradox in photodamaged skin

The 1979 Gilchrest study noted a finding that is central to understanding pigmentary ageing: despite declining overall numbers, the surviving melanocytes in chronically sun-exposed skin exhibited greater DOPA-positivity – a proxy for tyrosinase activity – than their counterparts in photoprotected skin from the same individual [5]. The surviving cells are individually more melanogenically active. This is not a paradox if understood as a compensation or dysregulation mechanism: as melanocyte density falls, those that remain become hyperactivated, producing more melanin per cell rather than less.

Under the influence of accumulated UV damage, keratinocytes in photodamaged epidermis also shift their paracrine signalling profile in ways that sustain and amplify melanocyte activity. Repeated UVB exposure has been shown to drive keratinocytes to produce -alpha (TNF-α), which in turn stimulates autocrine production of endothelin-1 (EDN-1) and stem cell factor (SCF) [8]. These paracrine mediators act on neighbouring melanocytes via the endothelin B receptor (EDNBR) and the receptor tyrosine kinase c-Kit, respectively. The sequential nature of this cascade is well characterised: SCF/c-Kit signalling predominates in the early phase of UV-induced melanogenesis, priming EDNBR expression on melanocytes; EDN-1/EDNBR signalling then drives the sustained, later-phase upregulation of MITF, tyrosinase, and melanin synthesis [6].

Solar lentigo formation

Solar lentigines – colloquially termed age spots – represent the most visible clinical consequence of this dysregulated paracrine loop operating in a spatially restricted context. Their formation is best understood not as a random event but as the focal persistence and amplification of the UV-activated keratinocyte-melanocyte signalling axis in discrete epidermal zones.

Gene expression profiling of solar lentigo biopsies compared with adjacent sun-exposed normal skin has identified upregulation of inflammation-related genes and melanocyte-associated markers (including TRP-1 positive cells in the basal layer), alongside notably reduced keratinocyte proliferation and cornification [1]. A subsequent microarray and immunohistochemical study found that increased basal keratinocyte proliferation combined with reduced suprabasal keratinocyte turnover is associated with the characteristic elongated rete ridges of solar lentigo – a structural change proposed to impair the normal upward dispersal of melanin-containing melanosomes from the basal layer [2]. The result is not purely greater melanin production but also melanin accumulation through disrupted clearance.

Whilst the EDN-1/SCF paracrine cascade is the principal driver of melanocyte activation within these lesions – as summarised from primary lentigo studies by [8] – the current body of evidence does not clearly support a monoclonal somatic mutation model for solar lentigo development. The available data are more consistent with a focal paracrine dysregulation model in which UV-primed keratinocytes establish a self-sustaining activating loop with neighbouring melanocytes. Whether this is initiated by a pre-existing population of UV-sensitive keratinocytes or reflects stochastic variation in paracrine signalling intensity across the epidermis remains incompletely understood.

Two distinct clinical phenotypes

The melanocyte ageing paradox thus produces two phenotypically and mechanistically distinct presentations in photodamaged skin:

  1. Generalised even-tone loss – reflecting overall melanocyte density decline; diffuse across sun-exposed areas; the underlying biology is cell attrition with residual cells that may be individually more active but too sparse to maintain even coverage.

  2. Focal hyperpigmentation (solar lentigines) – reflecting focal zones of keratinocyte-driven paracrine melanocyte overactivation, compounded by impaired melanosome dispersal via disrupted rete ridge architecture; discrete, circumscribed, and mechanistically distinct from the diffuse background pallor.

These two phenotypes frequently coexist in the same patient and in the same anatomical region, which explains the characteristic heterogeneous pigmentation of chronically sun-exposed older skin: generalised uneven tone punctuated by discrete darker lesions on a background of relative pallor elsewhere.

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Clinical Application

Melanocytes are central to two of the clinic’s core treatment categories – hair removal and pigmentation management – and understanding their biology gives both treatment conversations a precision that the standard “the laser targets pigment” framing doesn’t quite achieve.

Hair Removal: Why Melanin Is the Target

IPL and diode laser hair removal both operate through selective photothermolysis, the principle that a specific wavelength of light, delivered at the right pulse duration, will be preferentially absorbed by a target chromophore (in this case melanin) and convert to heat, destroying the follicle without equivalent damage to surrounding tissue. The melanin in the hair shaft and the matrix melanocytes of the lower follicle absorbs the energy; the heat generated is sufficient to damage the follicle’s regenerative capacity when the treatment is timed to the (active growth) phase, when melanocyte activity and melanin content are highest.

This mechanism has a direct implication for client selection and expectation-setting. The system works because of the contrast between melanin-rich follicle tissue and the surrounding less-pigmented dermis. Fair skin with dark hair produces the highest contrast and the most efficient energy delivery to the target. Dark skin with dark hair reduces that contrast – the risk of competing absorption in the surrounding epidermis requires adjusted fluence and pulse parameters. Light or grey hair has reduced melanin content in the follicle matrix, and significantly reduced or absent McSC-derived pigmentation in grey or white hair makes those follicles substantially less amenable to light-based removal. This is not a limitation to apologise for, it is a consequence of the precise mechanism being exploited, and explaining it honestly sets realistic expectations and builds confidence in the rationale.

The McSC depletion finding adds a useful nuance for clients with mixed dark and greying hair. Greying does not occur uniformly because melanocyte stem cell exhaustion progresses follicle by follicle; each follicle’s McSC pool depletes independently. A client presenting with predominantly dark hair in a target area but some grey will have variable melanin content across follicles, with the grey follicles essentially outside the reach of the treatment mechanism. Retreating as further follicles darken during a growth cycle (and before they progress to grey) is mechanistically justified.

Treatment Timing and the Hair Cycle

Because IPL and diode laser target the follicle at its most melanin-rich state, treatment is most effective during anagen. The proportion of follicles in anagen varies by body site – approximately 85% on the , 20–30% in axillary and bikini areas – which is why body site differences in treatment intervals and session numbers are not arbitrary but reflect the underlying follicle cycle biology. Scheduling intervals that account for cycle length at the target site maximises the proportion of follicles caught in their vulnerable phase across the treatment course.

Pigmentation: Treating Without Disrupting

For IPL in pigmentation management – sunspots, post-inflammatory hyperpigmentation, diffuse photodamage – the clinical context shifts from follicle destruction to selective melanocyte impact. Targeted energy absorption by melanin-dense lesions produces localised melanocyte disruption and melanin breakdown, with the treated pigment fragmenting and clearing over subsequent weeks.

The melanocyte density decline with age (approximately 10–20% per decade from the third decade) is worth bearing in mind for realistic outcome framing. Treating established solar lentigines in significantly photoaged skin is working with a melanocyte population that is already sparser, more irregularly distributed, and more likely to include senescent cells than in younger skin. Clearance is achievable but the surrounding skin’s capacity for even re-pigmentation thereafter is reduced. Managing expectations around longevity and maintenance intervals, particularly for clients with significant cumulative UV exposure, is part of honest treatment planning.

The MC1R/DNA repair signalling point is worth holding in the background for client education on photoprotection. UV damage to keratinocytes is partly mediated and repaired through the α-MSH → MC1R pathway activated by melanocytes, which means that anything that impairs melanocyte function (including advancing senescence and density decline) progressively reduces the epidermis’s own UV damage repair capacity. SPF is not just preventing visible pigmentation changes; it is protecting the signalling system that helps the skin repair UV-induced DNA damage in real time. That framing, particularly for clients who are sceptical about SPF’s importance beyond cosmetic evenness, tends to land more meaningfully than the standard “it prevents ageing” message.

Fitzpatrick Type and Treatment Safety

IPL and diode laser parameters must be adjusted for Fitzpatrick skin type precisely because higher epidermal melanin content in darker skin types competes for energy absorption with the target follicle melanin. For Fitzpatrick types IV–VI, diode laser at longer wavelengths (808–1064nm range) provides deeper penetration and reduced epidermal melanin competition compared to broadband IPL, reducing the risk of surface burns and post-inflammatory hyperpigmentation. Any treatment-induced epidermal disruption in darker skin types carries a higher risk of triggering the very melanocyte hyperactivity it is intended to address; another reason why precise parameter selection and thorough Fitzpatrick assessment sit at the front of the treatment consultation, not as a formality but as a direct safety consideration.

Distinguishing Generalised from Focal Pigmentation: Treatment Implications

Photodamaged skin in older patients commonly presents with both generalised even-tone decline and discrete focal hyperpigmentation, and these two presentations require different therapeutic reasoning even when they share the same anatomical distribution. Conflating them – treating age spots as though they were simply an intensified version of generalised photodamage – leads to suboptimal outcomes and occasionally to disappointment when a patient expects comprehensive rejuvenation from a single targeted session.

Generalised even-tone loss reflects the progressive decline in the overall melanocyte population, producing areas of relative hypomelanosis, textural irregularity, and a loss of luminosity. The underlying biology is attrition rather than focal activation: there are simply fewer melanocytes distributing pigment across the basal layer, and those that remain produce melanin unevenly. Treatment approaches for this phenotype are directed at skin quality as a whole rather than discrete lesions. Photoprotection is essential and, when started early, is expected to limit further attrition. Broad-field energy devices – particularly IPL used at lower fluences across a wider treatment area – can improve generalised even-tone by targeting diffuse melanin deposits in the upper dermis and epidermis. -stimulating treatments (radiofrequency, , /) address the concurrent dermal remodelling deficit, restoring the structural context within which melanocyte distribution appears more even. For patients with concurrent , the hormonal contribution to melanocyte regulation and barrier integrity warrants discussion.

Focal solar lentigines arise from a keratinocyte-driven paracrine loop that maintains discrete zones of melanocyte overactivation, compounded by altered rete ridge architecture that reduces melanin clearance from those zones. These lesions respond well to targeted energy delivery that selectively destroys the hyperpigmented chromophore. IPL is effective for superficial solar lentigines: melanin in these lesions absorbs preferentially at 515–590 nm, making them well-suited to selective photothermolysis. The endpoint is immediate darkening followed by superficial crusting and sloughing over 7–14 days. Q-switched Nd:YAG (1064 nm or frequency-doubled 532 nm) targets deeper or denser melanin and is particularly appropriate for patients with Fitzpatrick types III–IV where IPL carries a higher risk of post-inflammatory hyperpigmentation from non-selective thermal spread.

Pre-treatment assessment pointers. The clinical distinction between the two phenotypes guides device selection, but several assessment principles apply across both:

  • Establish the dominant phenotype. Ask: is the patient primarily concerned with overall brightness and even-tone, or with specific dark spots? If both, treat focal lesions first and reassess even-tone at follow-up when the visual noise of lesions is removed.

  • Fitzpatrick type is more predictive of risk with focal treatment than with broad-field treatment. For Fitzpatrick types III–IV, a conservative test patch for any IPL or laser lentigo treatment is mandatory; the risk of post-inflammatory hyperpigmentation following targeted energy delivery in darker skin types is substantially elevated.

  • Distinguish lentigo from lentigo maligna. Any lesion with border irregularity, colour heterogeneity, or rapid change should be referred for dermoscopic evaluation before treatment. Energy-based ablation of an undiagnosed lentigo maligna is a serious clinical error.

  • Solar lentigines on the dorsum of the hands behave differently from facial lesions – the skin is thinner, vascularity differs, and healing is slower. Adjust fluence and expect longer recovery.

  • Topical priming can support both presentations. pre-treatment reduces epidermal melanin load and improves energy device outcomes for focal lesions; broad-spectrum photoprotection immediately following treatment limits recurrence driven by the keratinocyte paracrine cascade.

For patients presenting with the combined picture – the heterogeneous photodamaged skin typical of the fifth decade and beyond – a sequenced approach often yields the most satisfying outcome: address focal lentigines in sessions one and two, then use broad-field skin-quality treatments to harmonise the surrounding diffuse photodamage. This sequence also allows accurate assessment of the generalised even-tone phenotype once the focal distraction of discrete lesions has resolved.

References

  1. Aoki H, Moro O, Tagami H, et al. (2007). Gene expression profiling analysis of solar lentigo in relation to immunohistochemical characteristics. Br J Dermatol, 156(6), 1214-23 .

  2. Choi W, Yin L, Smuda C, et al. (2017). Molecular and histological characterization of age spots. Exp Dermatol, 26(3), 242-248 .

  3. Dong L, Wen J, Pier E, et al. (2010). Melanocyte-stimulating hormone directly enhances UV-Induced DNA repair in keratinocytes by a xeroderma pigmentosum group A-dependent mechanism. Cancer Res, 70(9), 3547-56 .

  4. García-Borrón JC, Abdel-Malek Z, Jiménez-Cervantes C (2014). MC1R, the cAMP pathway, and the response to solar UV: extending the horizon beyond pigmentation. Pigment Cell Melanoma Res, 27(5), 699-720 .

  5. Gilchrest BA, Blog FB, Szabo G (1979). Effects of aging and chronic sun exposure on melanocytes in human skin. J Invest Dermatol, 73(2), 141-3 .

  6. Hachiya A, Kobayashi A, Yoshida Y, et al. (2004). Biphasic expression of two paracrine melanogenic cytokines, stem cell factor and endothelin-1, in ultraviolet B-induced human melanogenesis. Am J Pathol, 165(6), 2099-109 .

  7. Hartman ML, Czyz M (2015). MITF in melanoma: mechanisms behind its expression and activity. Cell Mol Life Sci, 72(7), 1249-60 .

  8. Imokawa G (2019). Melanocyte Activation Mechanisms and Rational Therapeutic Treatments of Solar Lentigos. Int J Mol Sci, 20(15) .

  9. Levy C, Khaled M, Fisher DE (2006). MITF: master regulator of melanocyte development and melanoma oncogene. Trends Mol Med, 12(9), 406-14 .

  10. Manganelli M, Guida S, Ferretta A, et al. (2021). Behind the Scene: Exploiting MC1R in Skin Cancer Risk and Prevention. Genes (Basel), 12(7) .

  11. Ortonne JP (1990). Pigmentary changes of the ageing skin. Br J Dermatol, 122 Suppl 35, 21-8 .

  12. Pang S, Wu H, Wang Q, et al. (2014). Chronic stress suppresses the expression of cutaneous hypothalamic-pituitary-adrenocortical axis elements and melanogenesis. PLoS One, 9(5), e98283 .

  13. Pasquali E, García-Borrón JC, Fargnoli MC, et al. (2015). MC1R variants increased the risk of sporadic cutaneous melanoma in darker-pigmented Caucasians: a pooled-analysis from the M-SKIP project. Int J Cancer, 136(3), 618-31 .

  14. Ploper D, Taelman VF, Robert L, et al. (2015). MITF drives endolysosomal biogenesis and potentiates Wnt signaling in melanoma cells. Proc Natl Acad Sci U S A, 112(5), E420-9 .

  15. Skobowiat C, Dowdy JC, Sayre RM, et al. (2011). Cutaneous hypothalamic-pituitary-adrenal axis homolog: regulation by ultraviolet radiation. Am J Physiol Endocrinol Metab, 301(3), E484-93 .

  16. Slominski A, Wortsman J, Luger T, et al. (2000). Corticotropin releasing hormone and proopiomelanocortin involvement in the cutaneous response to stress. Physiol Rev, 80(3), 979-1020 .

  17. Sun Q, Lee W, Hu H, et al. (2023). Dedifferentiation maintains melanocyte stem cells in a dynamic niche. Nature, 616(7958), 774-782 .

  18. Victorelli S, Lagnado A, Halim J, et al. (2019). Senescent human melanocytes drive skin ageing via paracrine telomere dysfunction. EMBO J, 38(23), e101982 .

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