ArticleJournal of bioenergetics and biomembranes2026
ATF5 reduces LPS-induced cardiac injury by modulating pyroptosis via mitophagy.
Article in Journal of bioenergetics and biomembranes, 2026. 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
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocarditis, often triggered by infections such as sepsis, involves complex mechanisms including mitochondrial dysfunction, oxidative stress and inflammation. The role of activating transcription factor 5 (ATF5) in myocarditis remains unclear. This study aimed to investigate the role of ATF5 in LPS-induced cardiac injury and its potential mechanism involving mitophagy and pyroptosis. An LPS-induced septic cardiomyopathy model was established in H9c2 cardiomyocytes and rats. ATF5 was overexpressed via plasmid transfection in vitro and in vivo. Cell viability, apoptosis, inflammatory cytokine levels, oxidative stress markers, mitophagy-related proteins (LC3-II, Parkin, PINK1, p62), and pyroptosis-related proteins (NLRP3, Caspase-1, GSDMD) were assessed using CCK-8, flow cytometry, ELISA, Western blot, and biochemical assays. Autophagy inhibitor chloroquine (CQ) and GSDMD-targeted siRNA were applied to explore mechanistic interactions. The results showed that ATF5 overexpression alleviated LPS-induced cardiomyocyte injury by enhancing cell viability, reducing apoptosis, and suppressing inflammatory cytokine release (IL-1β, IL-6 and IL-18) and myocardial injury markers (CK-MB and cTn-I). ATF5 promoted mitophagy, reduced oxidative stress (ROS, LDH, GSH-Px and SOD), and inhibited pyroptosis. Mechanistically, CQ abolished the ATF5-mediated protection against cardiomyocyte injury, which was then restored by si-GSDMD. In vivo, ATF5 overexpression improved cardiac function, attenuated fibrosis and decreased serum injury markers in LPS-treated rats. In conclusion, ATF5 enhanced mitophagy, effectively cleared damaged mitochondria, reduced ROS generation, and subsequently inhibited the pyroptosis pathway, ultimately alleviating myocardial injury.
Indexed as
Identifiers
42209853What 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.