Dysfunction of Autophagy: A Possible Mechanism Involved in the Pathogenesis of Vitiligo by Breaking the Redox Balance of Melanocytes.

PubWeight™: 0.75‹?›

🔗 View Article (PMID 28018522)

Published in Oxid Med Cell Longev on November 29, 2016

Authors

Zhuhui Qiao1, Xiuxiu Wang1, Leihong Xiang1, Chengfeng Zhang1

Author Affiliations

1: Department of Dermatology, Huashan Hospital, Fudan University, Shanghai, China.

Articles cited by this

Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice. Cell (2007) 14.63

Cell survival responses to environmental stresses via the Keap1-Nrf2-ARE pathway. Annu Rev Pharmacol Toxicol (2007) 12.48

Autophagy: renovation of cells and tissues. Cell (2011) 11.59

Direct evidence that sulfhydryl groups of Keap1 are the sensors regulating induction of phase 2 enzymes that protect against carcinogens and oxidants. Proc Natl Acad Sci U S A (2002) 8.01

The selective autophagy substrate p62 activates the stress responsive transcription factor Nrf2 through inactivation of Keap1. Nat Cell Biol (2010) 6.95

p62 at the crossroads of autophagy, apoptosis, and cancer. Cell (2009) 5.97

A noncanonical mechanism of Nrf2 activation by autophagy deficiency: direct interaction between Keap1 and p62. Mol Cell Biol (2010) 2.93

Clinical practice. Vitiligo. N Engl J Med (2009) 2.72

Autophagy in immunity and cell-autonomous defense against intracellular microbes. Immunol Rev (2011) 2.58

Molecular basis for the contribution of the antioxidant responsive element to cancer chemoprevention. Cancer Lett (2001) 2.57

Eighty-six cases of Addison's disease. Clin Endocrinol (Oxf) (1994) 2.19

NBR1 and p62 as cargo receptors for selective autophagy of ubiquitinated targets. Cell Cycle (2009) 2.12

Low catalase levels in the epidermis of patients with vitiligo. J Invest Dermatol (1991) 1.89

Vitiligo: interplay between oxidative stress and immune system. Exp Dermatol (2013) 1.85

Profile of alopecia areata in Northern India. Int J Dermatol (1996) 1.64

Genome-wide siRNA-based functional genomics of pigmentation identifies novel genes and pathways that impact melanogenesis in human cells. PLoS Genet (2008) 1.64

In vivo and in vitro evidence for hydrogen peroxide (H2O2) accumulation in the epidermis of patients with vitiligo and its successful removal by a UVB-activated pseudocatalase. J Investig Dermatol Symp Proc (1999) 1.58

On the etiology of contact/occupational vitiligo. Pigment Cell Res (2004) 1.55

Role of Nrf2 signaling in regulation of antioxidants and phase 2 enzymes in cardiac fibroblasts: protection against reactive oxygen and nitrogen species-induced cell injury. FEBS Lett (2005) 1.53

Vitiligo: compendium of clinico-epidemiological features. Indian J Dermatol Venereol Leprol (2007) 1.46

Vitiligo puzzle: the pieces fall in place. Pigment Cell Res (2007) 1.39

Vitiligo pathogenesis: autoimmune disease, genetic defect, excessive reactive oxygen species, calcium imbalance, or what else? Exp Dermatol (2008) 1.39

A critical appraisal of vitiligo etiologic theories. Is melanocyte loss a melanocytorrhagy? Pigment Cell Res (2003) 1.27

The significance of Nrf2 pathway in (photo)-oxidative stress response in melanocytes and keratinocytes of the human epidermis. Pigment Cell Melanoma Res (2008) 1.24

Autophagy in immunity: implications in etiology of autoimmune/autoinflammatory diseases. Autophagy (2012) 1.16

Melanocytes as instigators and victims of oxidative stress. J Invest Dermatol (2014) 1.13

NF-E2-related factor 2 regulates the stress response to UVA-1-oxidized phospholipids in skin cells. FASEB J (2009) 1.13

Heme oxygenase-1 protects human melanocytes from H2O2-induced oxidative stress via the Nrf2-ARE pathway. J Invest Dermatol (2011) 1.09

Neurogenic dysregulation, oxidative stress, autoimmunity, and melanocytorrhagy in vitiligo: can they be interconnected? Pigment Cell Res (2007) 1.08

Oxidized proteins: mechanisms of removal and consequences of accumulation. IUBMB Life (2009) 1.08

A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol (2012) 1.06

Vitiligo: pathogenetic hypotheses and targets for current therapies. Curr Drug Metab (2010) 1.01

Impaired activation of the Nrf2-ARE signaling pathway undermines H2O2-induced oxidative stress response: a possible mechanism for melanocyte degeneration in vitiligo. J Invest Dermatol (2014) 0.99

Higher plasma catecholamine and metabolite levels in the early phase of nonsegmental vitiligo. Pigment Cell Res (2000) 0.98

Melanocyte detachment after skin friction in non lesional skin of patients with generalized vitiligo. Br J Dermatol (2003) 0.95

The pleiotropic roles of autophagy regulators in melanogenesis. Pigment Cell Melanoma Res (2011) 0.92

Suppression of autophagy dysregulates the antioxidant response and causes premature senescence of melanocytes. J Invest Dermatol (2014) 0.92

Transcriptional upregulation of Nrf2-dependent phase II detoxification genes in the involved epidermis of vitiligo vulgaris. J Invest Dermatol (2010) 0.91

The susceptibility to vitiligo is associated with NF-E2-related factor2 (Nrf2) gene polymorphisms: a study on Chinese Han population. Exp Dermatol (2008) 0.90

Autophagy has a significant role in determining skin color by regulating melanosome degradation in keratinocytes. J Invest Dermatol (2013) 0.90

Autophagy is induced by UVA and promotes removal of oxidized phospholipids and protein aggregates in epidermal keratinocytes. J Invest Dermatol (2013) 0.90

Decreased methionine sulphoxide reductase A expression renders melanocytes more sensitive to oxidative stress: a possible cause for melanocyte loss in vitiligo. Br J Dermatol (2009) 0.89

Role of oxidative stress and autoimmunity in onset and progression of vitiligo. Exp Dermatol (2014) 0.88

Difference in pathogenesis between vitiligo vulgaris and halo nevi associated with vitiligo is supported by an HLA association study. Pigment Cell Res (2004) 0.88

Calcineurin suppresses AMPK-dependent cytoprotective autophagy in cardiomyocytes under oxidative stress. Cell Death Dis (2014) 0.87

Autophagy induced by resveratrol suppresses α-MSH-induced melanogenesis. Exp Dermatol (2014) 0.87

Vitiligo in Graves' disease. Ann Intern Med (1969) 0.86

Increased expression of CXCR3 and its ligands in patients with vitiligo and CXCL10 as a potential clinical marker for vitiligo. Br J Dermatol (2016) 0.85

Oxidative stress in melanocyte senescence and melanoma transformation. Eur J Cell Biol (2013) 0.85

Methionine sulfoxide reductases A and B are deactivated by hydrogen peroxide (H2O2) in the epidermis of patients with vitiligo. J Invest Dermatol (2007) 0.85

Ultrastructural and functional alterations of mitochondria in perilesional vitiligo skin. J Dermatol Sci (2009) 0.84

Keratinocytes act as a source of reactive oxygen species by transferring hydrogen peroxide to melanocytes. J Invest Dermatol (2005) 0.84

The role of transcription factor Nrf2 in skin cells metabolism. Arch Dermatol Res (2015) 0.83

Membrane lipid alterations as a possible basis for melanocyte degeneration in vitiligo. J Invest Dermatol (2007) 0.82

Highlights in pathogenesis of vitiligo. World J Clin Cases (2015) 0.82

Membrane lipid defects are responsible for the generation of reactive oxygen species in peripheral blood mononuclear cells from vitiligo patients. J Cell Physiol (2010) 0.81

H(2)O(2) increases de novo synthesis of (6R)-L-erythro-5,6,7,8-tetrahydrobiopterin via GTP cyclohydrolase I and its feedback regulatory protein in vitiligo. J Inherit Metab Dis (2008) 0.80

Dysfunction of glutathione S-transferase leads to excess 4-hydroxy-2-nonenal and H(2)O(2) and impaired cytokine pattern in cultured keratinocytes and blood of vitiligo patients. Antioxid Redox Signal (2010) 0.80

Evidence that geniposide abrogates norepinephrine-induced hypopigmentation by the activation of GLP-1R-dependent c-kit receptor signaling in melanocyte. J Ethnopharmacol (2008) 0.78

Comparison of oxidant-antioxidant status in patients with vitiligo and healthy population. Kathmandu Univ Med J (KUMJ) (2015) 0.78

Vitiligo: Pathogenesis, clinical variants and treatment approaches. Autoimmun Rev (2015) 0.77

Oxidation levels differentially impact melanocytes: low versus high concentration of hydrogen peroxide promotes melanin synthesis and melanosome transfer. Dermatology (2012) 0.77

Genetic polymorphism of the Nrf2 promoter region is associated with vitiligo risk in Han Chinese populations. J Cell Mol Med (2016) 0.76

[Oxidative stress and aging]. Ugeskr Laeger (2000) 0.76

Autophagy as a melanocytic self-defense mechanism. J Invest Dermatol (2015) 0.76