ReviewMolecular medicine reports2022
Cardiomyocyte death in sepsis: Mechanisms and regulation (Review).
Review in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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
24 citing papers in PubMed, 53 citations in OpenAlex.
- Short-term blockade of E-prostanoid 3 receptor mitigates necroinflammation and ameliorates ischemia/reperfusion- and doxorubicin-induced acute myocardial injury.Basic research in cardiology · 2026Article
- Emerging biomodels to understand the pathophysiology of sepsis and evaluate new therapeutic strategies targeting extracellular histones.Materials today. Bio · 2026Review
- mRedox biology · 2026Review
- Septic Cardiomyopathy in the ICU: Echocardiographic Phenotypes, Global Longitudinal Strain, and Right Ventricular Assessment.Diagnostics (Basel, Switzerland) · 2026Review
- Association Between Myocardial Dysfunction and Septic Shock.International journal of molecular sciences · 2026Review
- Autophagy-ferroptosis crosstalk in sepsis: metabolic pathways, redox injury, and host-directed antioxidant nanomedicine.Frontiers in immunology · 2026Review
- PCSK9 inhibition alleviates sepsis-induced myocardial dysfunction by facilitating PINK1/parkin-associated mitophagy.Frontiers in pharmacology · 2026Article
- The Role of Pyroptosis in Exacerbating Sepsis-Induced Myocardial Injury: Mechanisms and Implications.Journal of inflammation research · 2026Review
- Progress on Potential Therapeutic Targets for Sepsis-Related Cardiac Dysfunction: From Basic Research to Clinical Translation.ImmunoTargets and therapy · 2026Review
- Sepsis-related myocardial injury: the role of bacterial pathogens and toxins-a scoping review protocol.BMJ open · 2025Article
- Roles and Therapeutic Targeting of Exosomes in Sepsis-Induced Cardiomyopathy.Journal of cellular and molecular medicine · 2025Review
- FermentedNutrients · 2025Article
- N6-Methyladenosine Demethylase ALKBH5 Promotes Pyroptosis by Modulating PTBP1 mRNA Stability in LPS-Induced Myocardial Dysfunction.Acta Cardiologica Sinica · 2024Article
- Molecular hydrogen attenuates sepsis-induced cardiomyopathy in mice by promoting autophagy.BMC anesthesiology · 2024Article
- Septic Cardiomyopathy.Reviews in cardiovascular medicine · 2024Review
- Article
- Dexmedetomidine regulates exosomal miR-29b-3p from macrophages and alleviates septic myocardial injury by promoting autophagy in cardiomyocytes via targeting glycogen synthase kinase 3β.Burns & trauma · 2024Article
- Levosimendan for sepsis-induced myocardial dysfunction: friend or foe?Frontiers in cardiovascular medicine · 2024Review
- Phospholipid transfer protein ameliorates sepsis-induced cardiac dysfunction through NLRP3 inflammasome inhibition.Open medicine (Warsaw, Poland) · 2024Article
- Klotho activation of Nrf2 inhibits the ferroptosis signaling pathway to ameliorate sepsis-associated acute kidney injury.Translational andrology and urology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Sepsis‑induced cardiac dysfunction is one of the most common types of organ dysfunction in sepsis; its pathogenesis is highly complex and not yet fully understood. Cardiomyocytes serve a key role in the pathophysiology of cardiac function; due to the limited ability of cardiomyocytes to regenerate, their loss contributes to decreased cardiac function. The activation of inflammatory signalling pathways affects cardiomyocyte function and modes of cardiomyocyte death in sepsis. Prevention of cardiomyocyte death is an important therapeutic strategy for sepsis‑induced cardiac dysfunction. Thus, understanding the signalling pathways that activate cardiomyocyte death and cross‑regulation between death modes are key to finding therapeutic targets. The present review focused on advances in understanding of sepsis‑induced cardiomyocyte death pathways, including apoptosis, necroptosis, mitochondria‑mediated necrosis, pyroptosis, ferroptosis and autophagy. The present review summarizes the effect of inflammatory activation on cardiomyocyte death mechanisms, the diversity of regulatory mechanisms and cross‑regulation between death modes and the effect on cardiac function in sepsis to provide a theoretical basis for treatment of sepsis‑induced cardiac dysfunction.
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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.