ArticleMolecular medicine reports2019
E3 ligase Fbw7 participates in oxidative stress‑induced myocardial cell injury via interacting with Mcl‑1.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Roles of Cullin-RING Ubiquitin Ligases in Cardiovascular Diseases.Biomolecules · 2022Review
- KLRD1, FOSL2 and LILRB3 as potential biomarkers for plaques progression in acute myocardial infarction and stable coronary artery disease.BMC cardiovascular disorders · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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Abstract
Oxidative stress participates in several heart diseases and is an important mechanism contributing to the pathological alterations of myocardial cell injury. In recent years, ubiquitylation has been demonstrated to be an important biochemical reaction associated with apoptosis. To investigate the effects and interactions of the E3 ligase F‑box and WD repeat domain containing 7 (Fbw7) and MCL1 apoptosis regulator, BCL2 family member (Mcl‑1) in myocardial cells during oxidative stress, Cell Counting Kit‑8, flow cytometry, western blot, reactive oxygen species and co‑immunoprecipitation assays were conducted. The current study revealed that Fbw7 may facilitate apoptosis via the Mcl‑1‑Bax pathway in oxidative stress‑induced myocardial H9c2 cell injury. Mcl‑1 inhibits the functions of Bcl‑2 family members, including the mitochondrial apoptosis factor Bax, to maintain cell viability; however, the present study suggested that Fbw7 may degrade Mcl‑1 and impaired this process. Therefore, it may be hypothesized that Fbw‑7 promotes myocardial cell injury via interacting with Mcl‑1.
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