ReviewAmerican journal of translational research2026
Roles of autophagy in sepsis-induced myocardial dysfunction: a comprehensive review.
Review in American journal of translational research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Mitochondrial dysfunction and the regulatory cell death crosstalk network in chronic obstructive pulmonary disease: from oxidative stress mechanisms to targeted therapeutic strategies.Frontiers in immunology · 2026Review
- Toll-like receptors in infectious myocarditis: pathogen-specific recognition, spatiotemporal dynamic regulation and clinical translation.Frontiers in cardiovascular medicine · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis-induced myocardial dysfunction (SIMD) is a worldwide health issue. Regarding malignant cardiac dysfunction and mortality, the fatality rate of SIMD accounts for 70-90%. The molecular mechanisms that underlie the inflammatory effects and cardiac function of SIMD appear to be intricate. A crucial cellular process associated with cardiomyopathy is the death of cardiomyocytes. In the review, we have summarized the present evidence on the role of autophagy in the pathomechanism of SIMD. The included studies suggest that cardiomyocyte death induced by SIMD might be partially regulated by autophagy and its associated genes and pathways, including but not limited to Unc-51 like-autophagy-activating kinase 1 (ULK1), Zinc finger antisense 1 (ZFAS1), miR-590-3p, miR-214-3p, miR-21-3p, Silent information regulator 1 (SIRT1), SH3 domain-containing protein 2 (SORBS2), AMP-activated protein kinase (AMPK), Mammalian target of rapamycin (mTOR), TLR4/ERK1/2/NF-κB, TFEB-CLEAR, and Tensin homolog deleted on chromosome 10/Protein kinase B (PTEN/AKT) pathway. The crosstalk among autophagy and its associated genes it might be one of the pivotal molecular and cellular mechanisms for SIMD. In addition, some interventions for treating SIMD, e.g. exogenous fibroblast growth factor 21, melatonin, urolithin A, and minocycline, were reported to be associated with their effects on the regulation of autophagy. However, due to limited research, the potential molecular mechanism underlying autophagy in regulating SIMD is unclear and requires further exploration through in vitro and in vivo experiments. Overall, a deeper understanding of SIMD pathogenesis may facilitate new prospects of therapeutic applications targeted to autophagy.
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.