Pathogenetic mechanisms of retinal degeneration include cell loss by apoptosis. This gene-regulated mode of single-cell death occurs in a number of widespread human diseases such as neurodegeneration. The knowledge of genes and signaling in retinal apoptosis is expanding and opens up therapeutic strategies to ameliorate blinding retinal diseases.

Download full-text PDF

Source
http://dx.doi.org/10.1152/physiologyonline.2000.15.3.120DOI Listing

Publication Analysis

Top Keywords

apoptosis retina
4
retina silent
4
silent death
4
death vision
4
vision pathogenetic
4
pathogenetic mechanisms
4
mechanisms retinal
4
retinal degeneration
4
degeneration include
4
include cell
4

Similar Publications

Aim: To explore the neuroprotective effects of high mobility group box 2 () knockdown on retinal ganglion cells (RGCs) in the retinal ischemia-reperfusion injury (RIRI).

Methods: Oxygen-glucose deprivation (OGD)-injured RGCs from postnatal three-day C57BL/6 mice pups and high intraocular pressure (IOP)-induced RIRI mice were used as cellular and animal models of RIRI. The expression of HMGB2 in the retina of RIRI mice and OGD-injured RGCs was detected through reverse transcription-polymerase chain reaction (RT-qPCR) and Western blotting.

View Article and Find Full Text PDF

Microglia, the parenchymal macrophage of the central nervous system, serve crucial remodeling functions throughout development. Microglia are transcriptionally heterogenous, suggesting that distinct microglial states confer discrete roles. Currently, little is known about how dynamic these states are, the cues that promote them, or how they impact microglial function.

View Article and Find Full Text PDF

SMTP-44D alleviates diabetic retinopathy by suppressing inflammation and oxidative stress in in vivo and in vitro models.

J Pharmacol Sci

February 2025

Department of Pharmacology, Showa University Graduate School of Pharmacy, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan; Pharmacological Research Center, Showa University, 1-5-8 Hatanodai, Shinagawa-ku, Tokyo, 142-8555, Japan.

Diabetic retinopathy (DR) is the leading cause of blindness among working-age adults, and inflammation and oxidative stress contribute to DR development. However, no effective treatments are currently approved for DR. Therefore, this study aimed to investigate the effects of SMTP-44D-a Stachybotrys microspora-derived compound with anti-inflammatory and antioxidant properties-on DR in in vivo and in vitro models.

View Article and Find Full Text PDF

Voltage-dependent anion channel 1 oligomerization regulates PANoptosis in retinal ischemia-reperfusion injury.

Neural Regen Res

January 2025

Department of Human Anatomy and Neurobiology, School of Basic Medical Science, Central South University, Changsha, Hunan Province, China.

Ischemia-reperfusion injury is a common pathophysiological mechanism in retinal degeneration. PANoptosis is a newly defined integral form of regulated cell death that combines the key features of pyroptosis, apoptosis, and necroptosis. Oligomerization of mitochondrial voltage-dependent anion channel 1 is an important pathological event in regulating cell death in retinal ischemia-reperfusion injury.

View Article and Find Full Text PDF

Age- and Sex-Specific Regulation of Serine Racemase in the Retina of an Alzheimer's Disease Mouse.

Invest Ophthalmol Vis Sci

January 2025

State Key Laboratory of Ophthalmology, Optometry, and Visual Science, Eye Hospital, Wenzhou Medical University, Wenzhou, China.

Purpose: Changes associated with Alzheimer's disease (AD) may have measurable effects on the retina, which may facilitate early detection due to the eye's accessibility. Retinal pathology and the regulation of serine racemase (SR) were investigated in the retinas of APP(SW)/PS1(∆E9) mice.

Methods: SR in the retinas and the content of D-serine in the aqueous humor were analyzed.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!