VDAC in Retinal Health and Disease

Biomolecules, Journal Year: 2024, Volume and Issue: 14(6), P. 654 - 654

Published: June 4, 2024

The retina, a tissue of the central nervous system, is vital for vision as its photoreceptors capture light and transform it into electrical signals, which are further processed before they sent to brain be interpreted images. retina unique in that continuously exposed has highest metabolic rate demand energy amongst all tissues body. Consequently, very susceptible oxidative stress. VDAC, pore outer membrane mitochondria, shuttles metabolites between mitochondria cytosol normally protects cells from damage, but when cell’s integrity greatly compromised initiates cell death. There three isoforms existing evidence indicates expressed retina. However, their precise localization function each type unknown. It appears most retinal express substantial amounts VDAC2 VDAC3, presumably protect them Photoreceptors VDAC2, HK2, PKM2—key proteins Warburg pathway also these cells. Consistent with role initiating death, VDAC overexpressed degenerative diseases retinitis pigmentosa, age related macular degeneration (AMD), glaucoma. Treatment antioxidants or inhibiting oligomerization reduced expression improved survival. Thus, may promising therapeutic candidate treatment diseases.

Language: Английский

Absence of oncomodulin increases susceptibility to noise-induced outer hair cell death and alters mitochondrial morphology

Frontiers in Neurology, Journal Year: 2024, Volume and Issue: 15

Published: Oct. 23, 2024

Cochlear outer hair cells (OHCs) play a fundamental role in the hearing sensitivity and frequency selectivity of mammalian are especially vulnerable to noise-induced damage. The OHCs depend on Ca 2+ homeostasis, which is balance between influx extrusion, as well buffering by proteins organelles. Alterations OHC homeostasis not only an immediate response noise, but also associated with impaired auditory function. However, there little known about contribution organelles vulnerability noise. In this study, we used knockout (KO) mouse model where oncomodulin ( Ocm ), major binding protein preferentially expressed OHCs, deleted. We show that KO mice were more susceptible noise induced loss compared wildtype (WT) mice. Following exposure (106 dB SPL, 2 h), had higher threshold shifts increased TUNEL staining, age-matched WT Mitochondrial morphology was significantly altered OHCs. Before exposure, showed decreased mitochondrial abundance, volume, branching measured immunocytochemical staining membrane protein, TOM20. barely visible Using cell culture prolonged cytosolic overload, OCM has protective effects against changes apoptosis. These experiments suggest disruption leads increase mitochondrial-associated

Language: Английский