ArticleInternational journal of cardiology. Cardiovascular risk and prevention2025
S100A4-shRNA mitigates autophagy, reduces inflammation, and improves cardiac functionality in MIRI.
Article in International journal of cardiology. Cardiovascular risk and prevention, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: S100A4 plays a crucial role in myocardial ischemia-reperfusion injury (MIRI), where the interplay between autophagy and inflammation shapes the progression of reperfusion injury. However, the specific mechanisms by which S100A4 influences autophagy and inflammation in this context remain unclear. Methods: An ischemia-reperfusion (I/R) model was established in mice. The optimal timing for inducing reperfusion injury was determined, and mice were divided into sham and experimental groups. The experimental group underwent 2 h of ischemia/reperfusion injury followed by a 2-day reperfusion period. In the I/R + S100A4-shRNA group, S100A4 silencing was achieved through the injection of short hairpin RNA (shRNA). Myocardial ischemia was induced by occluding the left anterior descending branch (LAD) of the coronary artery. Diagnostic procedures, including electrocardiogram assessments, cardiac function testing, cardiac enzyme analyses, and 2,3,5-triphenyl tetrazolium chloride (TTC) staining, were performed to assess myocardial injury. Immunohistochemistry, immunofluorescence staining, hematoxylin-eosin (HE) staining, and Masson trichrome staining were used to evaluate the expression levels of IL-1, TNF-a, morphological changes in cardiomyocytes, and cardiac fibrosis. Protein blotting was conducted to examine autophagy-related proteins and Bnip3 signaling-related proteins. Results: The study showed an increase in S100A4 expression, as well as upregulation of autophagy orchestrating proteins (Beclin-1 and LC3), contributing to myocardial injury and expansion of myocardial infarction (MI). S100A4 played a multifaceted role by regulating autophagy through the BNIP3 pathway in MIRI. Silencing S100A4 resulted in reduced autophagy and inflammation, leading to decreased infarct size and improved cardiac function. Conclusions: S100A4 is upregulated during MIRI and orchestrates autophagy through the BNIP3 pathway, influencing the progression of reperfusion injury following myocardial infarction. Inhibition of autophagy and mitigation of inflammatory responses by S100A4-shRNA provide protection against the detrimental effects of IRI on the heart.
Indexed as
Identifiers
What Socratic 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 Socratic graph.