The endoplasmic reticulum: Homeostasis and crosstalk in retinal health and disease

Zhang, Sarah X.; Wang, Josh J.; Starr, Christopher R.; Lee, Eun-Jin; Park, Karen Sophia; Zhylkibayev, Assylbek; Medina, Andy; Lin, Jonathan H.; Gorbatyuk, Marina

doi:10.1016/j.preteyeres.2023.101231

Cited by 3 publications

(1 citation statement)

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“…Liberated ATF6 moves to nucleus and activation, resulting in reduction of levels of damaged proteins and ERS levels. 39 These ER stress sensors are activated to trigger a controlled response to eliminate or adapt to ERS. Failure of the UPR in reestablishing ER homeostasis will result in cell death and disease progression ( Figure 1 ).…”

Section: Ermentioning

confidence: 99%

Endoplasmic Reticulum Dysfunction: An Emerging Mechanism of Vitiligo Pathogenesis

Xie,

Wu,

Tang

et al. 2024

CCID

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The endoplasmic reticulum (ER) is the main site of protein synthesis, transport, and modification. Its abnormal status has now emerged as an established cause of many pathological processes, such as tumors and autoimmune diseases. Recent studies also demonstrated that the defective functions of ER may lead to pigmentary diseases. Vitiligo is a depigmenting ailment skin disorder whose pathogenesis is now found to be associated with ER. However, the detailed mechanism is still unclear. In this review, we try to link the association between ER with its inter- and intra-organellar interactions in vitiligo pathogenesis and focus on the function, mechanism, and clinical potential of ER with vitiligo. Expand ER is found in melanocytes of vitiligo and ER stress (ERS) might be a bridge between oxidative stress and innate and adaptive immunity. Meanwhile, the tight association between ER and mitochondria or melanosomes in organelles levels, as well as genes and cytokines, is the new paradigm in the pathogenesis of vitiligo. This undoubtedly adds a new aspect to the understanding of vitiligo, facilitating the design of targeted therapies for vitiligo.

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Section: Ermentioning

confidence: 99%