ArticleAmerican journal of translational research2021
SYVN1/GPX5 axis affects ischemia/reperfusion induced apoptosis of AC16 cells by regulating ROS generation.
Article in American journal of translational research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Casting Light on the Janus-Faced HMG-CoA Reductase Degradation Protein 1: A Comprehensive Review of Its Dualistic Impact on Apoptosis in Various Diseases.Molecular neurobiology · 2024Review
- [Forsythiaside B inhibits cerebral ischemia/reperfusion-induced oxidative stress injury in miceNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Salvianolic acid B inhibits myocardial I/R-induced ROS generation and cell apoptosis by regulating the TRIM8/GPX1 pathway.Pharmaceutical biology · 2022Article
- Circular RNA circRNA-0039459 promotes the migration, invasion, and proliferation of liver cancer cells through the adsorption of miR-432.Bioengineered · 2022Article
- Article
- LncRNA MIAT enhances cerebral ischaemia/reperfusion injury in rat model via interacting with EGLN2 and reduces its ubiquitin-mediated degradation.Journal of cellular and molecular medicine · 2021Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischemia/reperfusion (I/R) induced injury is a major cause of coronary heart disease (CHD). Increased production of reactive oxygen species (ROS) can lead to an I/R injury in CHD, and the ROS level can be regulated by Glutathione peroxidase (GPX) enzyme family. In this study, we investigated the role and underlying molecular mechanism of GPX5 in I/R-induced AC16 cells. We found that the serum level of GPX5 was down-regulated in patients with CHD and I/R-induced AC16 cells. Overexpression of GPX5 inhibited I/R-induced apoptosis by suppressing the production of ROS. On the other hand, knock-down of GPX5 promoted apoptosis in AC16 cells by up-regulating the level of ROS. Furthermore, we found that GPX5 was regulated by synovial apoptosis inhibitor 1 (SYVN1)-mediated ubiquitination in AC16 cells. In I/R-induced AC16 cells, the expression of SYVN1 was up-regulated, and SYVN1 knock-down decreased the ROS levels and apoptotic rate but increased GPX5 levels. Moreover, GPX5 knockdown promoted ROS production and apoptosis, while its effects were attenuated by SYVN1 knockdown. Furthermore, SYVN1 was up-regulated while GPX5 was down-regulated in the myocardial tissue of I/R-injured rats. Taken together, our data demonstrate that GPX5 inhibits I/R-induced apoptosis of AC16 cells by down-regulating ROS level, and its stabilization is regulated by SYVN1-mediated ubiquitination.
Indexed as
Identifiers
34149998PMC8205806W3174868363What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.