ArticleScientific reports2025
SBK3 suppresses angiotensin II-induced cardiac hypertrophy by regulating mitochondrial metabolism.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Dysregulated Redox Signaling and Its Impact on Inflammatory Pathways, Mitochondrial Dysfunction, Autophagy and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Pathological cardiac hypertrophy is one of the risk factors for heart failure, characterized by elevated levels of renin-angiotensin II (Ang II) and catecholamines. SBK3 (SH3 domain binding kinase family member 3), a resident protein in the mitochondria, exhibits relatively high expression selectively in cardiac tissue based on human protein atlas database. Here, we studied the role of SBK3 in Ang II-induced cardiac hypertrophy to identify a new treatment for cardiac hypertrophy and heart failure by targeting mitochondria. The present study, for the first time, reveals the mitochondrial localization of SBK3 in rat cardiomyocytes and demonstrates a decrease in SBK3 protein expression in angiotensin II-perfused mice hearts. We found that maintaining high levels of SBK3 expression both in vivo and in vitro significantly suppressed Ang II-induced cardiac hypertrophy. This is attributed to the fact that overexpression of SBK3 rebalanced the levels of oxidative stress and energy metabolism induced by angiotensin II and inhibited the phosphorylation of dynamin-related protein 1 (Drp1) at the serine 616 site (S616) in cardiomyocytes and mice hearts. These findings suggest that SBK3 is a newly discovered mitochondrial protein capable of suppressing cardiac hypertrophy.
Indexed as
Identifiers
What 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.