Biochemical and Biophysical Research Communications, Journal Year: 2025, Volume and Issue: 749, P. 151385 - 151385
Published: Jan. 23, 2025
Language: Английский
Biochemical and Biophysical Research Communications, Journal Year: 2025, Volume and Issue: 749, P. 151385 - 151385
Published: Jan. 23, 2025
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(3), P. 894 - 894
Published: Jan. 22, 2025
Fuchs endothelial corneal dystrophy (FECD) is a progressive and debilitating disorder of the endothelium (CE) that affects approximately 4% individuals over age 40. Despite burden disease, pathogenesis FECD remains poorly understood, treatment options are limited, highlighting need for deeper investigation into its underlying molecular mechanisms. Over past decade, studies have indicated independent contributions endoplasmic reticulum (ER) mitochondrial stress to FECD. However, there limited suggesting ER-mitochondria crosstalk in Recently, our lab established role chronic ER inducing dysfunction cells (CEnCs), indicating existence This paper aims provide comprehensive overview current understanding how contribute pathogenesis. The also reviews literature on mechanisms other diseases relevant
Language: Английский
Citations
1Biochemical and Biophysical Research Communications, Journal Year: 2025, Volume and Issue: 749, P. 151385 - 151385
Published: Jan. 23, 2025
Language: Английский
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