Insights into the role of endoplasmic reticulum stress in skin function and associated diseases

Park, Kyungho; Lee, Sangeun; Shin, Kyong‐Oh; Uchida, Yoshikazu

doi:10.1111/febs.14739

Cited by 54 publications

(58 citation statements)

References 81 publications

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“…They explain how communication between the UPR and microbe‐sensing pathways can amplify cytokine production. This informs the discussions in several other articles of this Special Issue, including the review by Yoshikazu Uchida and colleagues on inflammatory skin conditions .…”

supporting

confidence: 56%

Endoplasmic reticulum stress: a key player in human disease

Marciniak

2019

The FEBS Journal

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This Special Issue comprises eleven excellent reviews that illustrate the role of ER stress in different human diseases, including myopathies and lung diseases, as well as in modulating liver dysfunction and inflammatory responses. These reviews also highlight the function of the UPR in neurodegenerative disorders and cancer, while discussing the potential benefits of targeting the UPR as a therapeutic approach. We hope you find these reviews interesting and informative and we thank the authors for these excellent contributions.

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supporting

confidence: 56%

Endoplasmic reticulum stress: a key player in human disease

Marciniak

2019

The FEBS Journal

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“…Emerging evidence has suggested that pharmacological targeting of ER stress can be an effective therapeutic strategy for treating tumors (34)(35)(36). Different natural compounds induced ER stress-mediated death in cancer cells (37). ER stress was also identified to serve a critical role in the pathogenesis of vitiligo (38)(39)(40).…”

Section: Discussionmentioning

confidence: 99%

RIPK1 regulates the survival of human melanocytes upon endoplasmic reticulum stress

et al. 2020

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Vitiligo is a common congenital or acquired disfiguring skin disorder. At present, endoplasmic reticulum (ER) stress has been identified to serve a critical role in the pathogenesis of vitiligo. Receptor-interacting serine/threonine-protein kinase 1 (RIPK1) is a protein serine/threonine kinase. The specific molecular mechanism of RIPK1 in human melanocytes upon ER stress remains to be determined. In the present study, RIPK1 was significantly downregulated in tunicamycin (TM)-induced ER stressed-human melanocytes. Subsequently, to explore the role of RIPK1 in ER stress-induced human melanocytes, human melanocytes were transfected with control or RIPK1 plasmids for 24 h and then treated with 3 µM TM for 48 h. Reverse transcription-quantitative PCR and western blot analysis indicated that the expression levels of protein kinase R-like endoplasmic reticulum kinase, eukaryotic translation initiation factor 2 subunit 1 and CCAAT-enhancer-binding protein homologous protein were significantly increased in the TM-treated group compared with the controls. In addition, the effect of high RIPK1 expression on ER stress-induced human melanocyte survival was studied. The present results indicated that TM inhibited cell viability and promoted apoptosis in human primary epidermal melanocytes. Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes. The effects of TM on human melanocytes were reversed by RIPK1 overexpression. Therefore, RIPK1 overexpression may have an effect on the PI3K/AKT/mTOR signaling pathway in human melanocytes under ER stress. The results of the current study demonstrated that RIPK1 could protect human melanocytes from cell damage induced by ER stress by regulating the PI3K/AKT/mTOR and ER stress signaling pathways, thereby serving a protective role in the occurrence and development of vitiligo.

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“…The transcription factor is constitutively expressed in all tissues [34]. Nrf2 functions at the interface of cellular redox and intermediary metabolism reactions as the target genes are involved in antioxidant enzyme production [35–37]. Nrf2 is a basic region leucine zipper transcription factor [38] that forms heterodimers in the nucleus of cells which recognises the enhancer sequence known as antioxidant response element (ARE).…”

Section: Oxidative Stressmentioning

confidence: 99%

Pathomechanisms of Blood-Brain Barrier Disruption in ALS

Kakaroubas

Brennan²,

Keon³

et al. 2019

Neuroscience Journal

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The blood-brain barrier (BBB) and the blood-spinal cord barrier (BSCB) are responsible for controlling the microenvironment within neural tissues in humans. These barriers are fundamental to all neurological processes as they provide the extreme nutritional demands of neural tissue, remove wastes, and maintain immune privileged status. Being a semipermeable membrane, both the BBB and BSCB allow the diffusion of certain molecules, whilst restricting others. In amyotrophic lateral sclerosis (ALS) and other neurodegenerative diseases, these barriers become hyperpermeable, allowing a wider variety of molecules to pass through leading to more severe and more rapidly progressing disease. The intention of this review is to discuss evidence that BBB hyperpermeability is potentially a disease driving feature in ALS and other neurodegenerative diseases. The various biochemical, physiological, and genomic factors that can influence BBB permeability in ALS and other neurodegenerative diseases are also discussed, in addition to novel therapeutic strategies centred upon the BBB.

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Insights into the role of endoplasmic reticulum stress in skin function and associated diseases

Cited by 54 publications

References 81 publications

Endoplasmic reticulum stress: a key player in human disease

Endoplasmic reticulum stress: a key player in human disease

RIPK1 regulates the survival of human melanocytes upon endoplasmic reticulum stress

Pathomechanisms of Blood-Brain Barrier Disruption in ALS

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