Publications by authors named "Yuecen Ding"

Vitiligo is a disfiguring depigmentation disorder characterized by loss of melanocytes. Although numerous studies have been conducted on the pathogenesis of vitiligo, the underlying mechanisms remain unclear. Although most studies have focused on melanocytes and keratinocytes, growing evidence suggests the involvement of dermal fibroblasts, residing deeper in the skin.

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Integrated skincare combines clinically proven skincare products with professional medical aesthetics to provide a comprehensive solution for beauty pursuers. Studies have demonstrated that a combination of medical aesthetic procedures and maintenance therapies is more effective than either treatment alone. This review outlines the current applications of integrated skincare, including different regimens of energy-based aesthetic devices and active ingredients in cosmeceuticals or chemical peels.

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Article Synopsis
  • - Riehl's melanosis is a skin condition characterized by hyperpigmentation, which can affect individuals psychologically and socially, and has seen new classification categories emerging over the past decade.
  • - The exact cause of Riehl's melanosis is uncertain, but it may involve factors like type IV hypersensitivity, genetics, UV exposure, and autoimmune responses, with various diagnostic tools available including dermoscopy and histopathology.
  • - Treatment options have improved and now include topical agents, oral medications, chemical peels, and advanced laser therapies, while recent research also explores biomarkers linked to this condition and other autoimmune diseases.
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Vitiligo is an acquired depigmentary disorder characterized by the depletion of melanocytes in the skin. Mitochondria shoulder multiple functions in cells, such as production of ATP, maintenance of redox balance, initiation of inflammation and regulation of cell death. Increasing evidence has implicated the involvement of mitochondria in the pathogenesis of vitiligo.

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Cysteine and glycine-rich protein 3 (CSRP3) is a striated muscle-specific cytoskeleton protein which participates in cardiac stretch sensing. Mutations in CSRP3 gene cause cardiomyopathies and deregulation of CSRP3 has been found in patients with heart failure and several skeletal muscle diseases. However, the mechanism underneath these disorders still remains poorly understood.

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