ABSTRACT
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. This review aims to elucidate the role of fibroblasts in both the physiological regulation of skin pigmentation and their pathological contribution to depigmentation, with the goal of shedding light on the involvement of fibroblasts in vitiligo. The topics covered in this review include alterations in the secretome, premature senescence, autophagy dysfunction, abnormal extracellular matrix, autoimmunity, and metabolic changes.
ABSTRACT
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. Mitochondria alteration will cause the abnormalities of mitochondria functions mentioned above, ultimately leading to melanocyte loss through various cell death modes. Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a critical role in mitochondrial homeostasis, and the downregulation of Nrf2 in vitiligo may correlate with mitochondria damage, making both mitochondria and Nrf2 promising targets in treatment of vitiligo. In this review, we aim to discuss the alterations of mitochondria and its role in the pathogenesis of vitiligo.
Subject(s)
Hypopigmentation , Vitiligo , Humans , Vitiligo/metabolism , NF-E2-Related Factor 2/metabolism , Oxidative Stress , Hypopigmentation/metabolism , Melanocytes/metabolism , Cell Death , Mitochondria/metabolism , Inflammation/metabolismABSTRACT
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. Additionally, the benefits and limitations of integrated skincare are discussed. Lastly, this review highlights the potential for improved satisfaction and long-term maintenance of the desired outcomes through appropriate integrated skincare procedures.
ABSTRACT
Riehl's melanosis is a hyperpigmentation disorder that has a significant psychological and social impact on individuals. In the past 10 years, new categories have been developed, raising questions about how to classify Riehl's melanosis. The mechanism of this disease remains unclear, although the type IV hypersensitivity response caused by allergic sensitization, as well as genetic, ultraviolet radiation, and autoimmune factors, is to blame. Clinical manifestation, dermoscopy, reflectance confocal microscopy, patch/photopatch testing, histopathology, and a novel multimodality skin imaging system have been used for the diagnosis. A variety of therapies including topical skin-lightening agents, oral tranexamic acid, glycyrrhizin compound, chemical peels, and lasers and light therapies (intense pulsed light, 1064-nm Q-Switched Nd: YAG laser, 755-nm PicoWay laser, nonablative 1927-nm fractional thulium fiber laser, new pulsed-type microneedling radiofrequency), with improved effectiveness. The latest findings on possible biomarkers and their relationship to other autoimmune diseases were also summarized.
Subject(s)
Melanosis , Tranexamic Acid , Humans , Ultraviolet Rays , Skin/pathology , Tranexamic Acid/therapeutic use , Glycyrrhizic Acid/therapeutic use , Melanosis/diagnosis , Melanosis/therapy , Treatment OutcomeABSTRACT
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. Here we generated the first csrp3 knockout zebrafish. csrp3-/- embryos showed no gross morphological defects but csrp3 deficient skeletal muscle fibers were prone to lesions upon prolonged stretching force. Further studies revealed csrp3 cooperatively interacted with ilk to maintain skeletal muscle mechanical stability and regulated tcap activation. Thus, our work has established a zebrafish model to investigate the function of csrp3 gene, and provides novel insights towards how csrp3 defects may lead to skeletal myopathies by a mechanistic link between Csrp3 and force stimuli.
