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DC Field Value Language Woo, Seung-Hwa - Mo, Yun Jeong - Lee, Yun-Il - Park, Ji Hwan - Hwang, Daehee - Park, Tae Jun - Kang, Hee Young - Park, Sang Chul - Lee, Young-Sam - 2023-10-23T18:10:18Z - 2023-10-23T18:10:18Z - 2023-07-13 - 2023-11 -
dc.identifier.issn 0022-202X -
dc.identifier.uri -
dc.description.abstract An effective healing response is critical to healthy aging. In particular, energy homeostasis has become increasingly recognized as a factor in effective skin regeneration. ANT2 is a mediator of adenosine triphosphate import into mitochondria for energy homeostasis. Although energy homeostasis and mitochondrial integrity are critical for wound healing, the role played by ANT2 in the repair process had not been elucidated to date. In our study, we found that ANT2 expression decreased in aged skin and cellular senescence. Interestingly, overexpression of ANT2 in aged mouse skin accelerated the healing of full-thickness cutaneous wounds. In addition, upregulation of ANT2 in replicative senescent human diploid dermal fibroblasts induced their proliferation and migration, which are critical processes in wound healing. Regarding energy homeostasis, ANT2 overexpression increased the adenosine triphosphate production rate by activating glycolysis and induced mitophagy. Notably, ANT2-mediated upregulation of HSPA6 in aged human diploid dermal fibroblasts downregulated proinflammatory genes that mediate cellular senescence and mitochondrial damage. This study shows a previously uncharacterized physiological role of ANT2 in skin wound healing by regulating cell proliferation, energy homeostasis, and inflammation. Thus, our study links energy metabolism to skin homeostasis and reports, to the best of our knowledge, a previously unreported genetic factor that enhances wound healing in an aging model. © 2023 The Authors -
dc.language English -
dc.publisher Elsevier B.V. -
dc.title ANT2 Accelerates Cutaneous Wound Healing in Aged Skin by Regulating Energy Homeostasis and Inflammation -
dc.type Article -
dc.identifier.doi 10.1016/j.jid.2023.05.002 -
dc.identifier.scopusid 2-s2.0-85162927549 -
dc.identifier.bibliographicCitation Journal of Investigative Dermatology, v.143, no.11, pp.2295 - 2310 -
dc.description.isOpenAccess TRUE -
dc.subject.keywordPlus CELLULAR SENESCENCE -
dc.subject.keywordPlus MITOCHONDRIAL PROTEIN -
dc.subject.keywordPlus DERMAL FIBROBLASTS -
dc.subject.keywordPlus DNA-DAMAGE -
dc.subject.keywordPlus STEM-CELLS -
dc.subject.keywordPlus CANCER -
dc.subject.keywordPlus PROLIFERATION -
dc.subject.keywordPlus MIGRATION -
dc.subject.keywordPlus DELIVERY -
dc.subject.keywordPlus HSP70 -
dc.citation.endPage 2310 -
dc.citation.number 11 -
dc.citation.startPage 2295 -
dc.citation.title Journal of Investigative Dermatology -
dc.citation.volume 143 -
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Appears in Collections:
Division of Biotechnology 1. Journal Articles
Department of New Biology Senescence-Associated Mechanism Lab 1. Journal Articles


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