ArticleThe Journal of investigative dermatology2015
Suppression of autophagy dysregulates the antioxidant response and causes premature senescence of melanocytes.
Article in The Journal of investigative dermatology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 2 of them syntheses that pooled it.
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Who cites it
58 citing papers in PubMed, 2 syntheses or guidelines pooled it, 114 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition).Autophagy · 2016Guideline
- Lymphoid Stress Surveillance Response Contributes to Vitiligo Pathogenesis.Frontiers in immunology · 2018Trial
- Dysregulated Intracellular Signaling in the Pathogenesis of Vitiligo: An Update on Emerging Therapeutic Strategies.Biomedicines · 2025Review
- Autophagy and Premature Graying of Hair: The Role of LC3 as a Biomarker in a Case-Control Study.Dermatology practical & conceptual · 2025Article
- Metabolic anomalies in vitiligo: a new frontier for drug repurposing strategies.Frontiers in pharmacology · 2025Article
- Interplay between MAPK signaling pathway and autophagy in skin aging: mechanistic insights and therapeutic implications.Frontiers in cell and developmental biology · 2025Review
- Imperatorin promotes melanin degradation in keratinocytes through facilitating autophagy via the PI3K/Akt signaling pathway.Archives of dermatological research · 2024Article
- ICP5249 Promotes Hair Growth by Activating the AMPK-Autophagy Signaling Pathway.Journal of microbiology and biotechnology · 2024Article
- USP3: Key deubiquitylation enzyme in human diseases.Cancer science · 2024Review
- The in vitro and in vivo depigmentation activity of coenzyme QCell communication and signaling : CCS · 2024Article
- The multifaceted role of autophagy in skin autoimmune disorders: a guardian or culprit?Frontiers in immunology · 2024Review
- Decreased ZMIZ1 suppresses melanogenesis in vitiligo by regulating mTOR/AKT/GSK-3β-mediated glucose uptake.In vitro cellular & developmental biology. Animal · 2024Article
- Elucidating the mechanisms and mitigation strategies for six-phthalate-induced toxicity in male germ cells.Frontiers in cell and developmental biology · 2024Article
- Vitiligo, from Pathogenesis to Therapeutic Advances: State of the Art.International journal of molecular sciences · 2023Review
- Reciprocal REGOxidative medicine and cellular longevity · 2023Article
- Cellular senescence: the good, the bad and the unknown.Nature reviews. Nephrology · 2022Review
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Authors and funding
14 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is the central cellular mechanism for delivering organelles and cytoplasm to lysosomes for degradation and recycling of their molecular components. To determine the contribution of autophagy to melanocyte (MC) biology, we inactivated the essential autophagy gene Atg7 specifically in MCs using the Cre-loxP system. This gene deletion efficiently suppressed a key step in autophagy, lipidation of microtubule-associated protein 1 light chain 3 beta (LC3), in MCs and induced slight hypopigmentation of the epidermis in mice. The melanin content of hair was decreased by 10-15% in mice with autophagy-deficient MC as compared with control animals. When cultured in vitro, MCs from mutant and control mice produced equal amounts of melanin per cell. However, Atg7-deficient MCs entered into premature growth arrest and accumulated reactive oxygen species (ROS) damage, ubiquitinated proteins, and the multi-functional adapter protein SQSTM1/p62. Moreover, nuclear factor erythroid 2-related factor 2 (Nrf2)-dependent expression of NAD(P)H dehydrogenase, quinone 1, and glutathione S-transferase Mu 1 was increased, indicating a contribution of autophagy to redox homeostasis in MCs. In summary, the results of our study suggest that Atg7-dependent autophagy is dispensable for melanogenesis but necessary for achieving the full proliferative capacity of MCs.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.