ArticleJournal of molecular histology2019
Sepsis-related myocardial injury is associated with Mst1 upregulation, mitochondrial dysfunction and the Drp1/F-actin signaling pathway.
Article in Journal of molecular histology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
- MicroRNAs as regulators of cardiac dysfunction in sepsis: pathogenesis and diagnostic potential.Frontiers in cardiovascular medicine · 2025Pooled it
- Sepsis-induced cardiomyopathy: mechanisms, epidemiology, diagnosis, and treatments.Frontiers in immunology · 2026Review
- MicroRNA-27b alleviates septic cardiomyopathy by targeting the Mff/MAVS axis.Frontiers in cellular and infection microbiology · 2025Article
- Pathogenesis and treatment strategies of sepsis-induced myocardial injury: modern and traditional medical perspectives.International journal of biological sciences · 2025Review
- Role and Mechanism of Mitochondrial Ribosomal Proteins in Septic Myocardial Injury.Journal of inflammation research · 2025Article
- Cardiac injury caused by iron overload in thalassemia.Frontiers in pediatrics · 2025Review
- Astragaloside IV Alleviates HCardiovascular therapeutics · 2025Article
- Review
- Mst1/Hippo signaling pathway drives isoproterenol-induced inflammatory heart remodeling.International journal of medical sciences · 2024Article
- Article
- MST1/2 in inflammation and immunity.Cell adhesion & migration · 2023Review
- LncRNA-mRNA expression profile and functional network of vascular dysfunction in septic rats.European journal of medical research · 2023Article
- RCAN1 deficiency aggravates sepsis-induced cardiac remodeling and dysfunction by accelerating mitochondrial pathological fission.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Research Progress on the Mechanism of Sepsis Induced Myocardial Injury.Journal of inflammation research · 2022Review
- Upregulation of miR‑335 exerts protective effects against sepsis‑induced myocardial injury.Molecular medicine reports · 2021Article
- Mitochondrial Dynamics: Pathogenesis and Therapeutic Targets of Vascular Diseases.Frontiers in cardiovascular medicine · 2021Review
- Comprehensive Mechanism, Novel Markers and Multidisciplinary Treatment of Severe Acute Pancreatitis-Associated Cardiac Injury - A Narrative Review.Journal of inflammation research · 2021Review
- It takes two to tango: coupling of Hippo pathway and redox signaling in biological process.Cell cycle (Georgetown, Tex.) · 2020Review
- SirT3 activates AMPK-related mitochondrial biogenesis and ameliorates sepsis-induced myocardial injury.Aging · 2020Article
- Identification of circRNA and mRNA expression profiles and functional networks of vascular tissue in lipopolysaccharide-induced sepsis.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LPS-induced septic cardiomyopathy has been found to be connected with mitochondrial stress through unknown mechanisms. Mitochondrial fission is an early event in mitochondrial dysfunction. The aim of our study was to determine the role and regulatory mechanism of mitochondrial fission in the progression of LPS-induced septic cardiomyopathy, with a particular focus on Mst1 and F-actin. Our data demonstrated that Mst1 expression was rapidly upregulated in LPS-treated hearts and that increased Mst1 promoted cardiomyocyte death by inducing mitochondrial stress. Mechanistically, elevated expression of Mst1 upregulated Drp1, and the latter initiated mitochondrial fission. Excessive mitochondrial fission caused mitochondrial oxidative injury, mitochondrial membrane potential reduction, mitochondrial proapoptotic element translocation into the cytoplasm/nucleus, mitochondrial energy dysfunction and mitochondrial apoptosis activation. Inhibition of mitochondrial fission sustained mitochondrial function and favored cardiomyocyte survival. Furthermore, we identified F-actin degradation as an apparent downstream event of mitochondrial fission activation in the context of LPS-induced septic cardiomyopathy. Stabilization of F-actin attenuated fission-mediated cardiomyocyte death. Altogether, our results define the Mst1/Drp1/mitochondrial fission/F-actin axis as a new signaling pathway that mediates LPS-related septic cardiomyopathy by inducing mitochondrial stress and cardiomyocyte death. Therefore, Mst1 expression, mitochondrial fission modification and F-actin stabilization may serve as potential therapeutic targets for sepsis-related myocardial injury.
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.