ArticleMolecular medicine reports2021
Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis.
Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The role of insulin resistance in hyperglycemia following cardiopulmonary resuscitation in rats.Resuscitation plus · 2026Article
- SS-31 improves post-cardiac arrest brain injury by inhibiting microglial ferroptosis and polarization.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Transplantation of exogenous mitochondria mitigates myocardial dysfunction after cardiac arrest.eLife · 2025Article
- Mitochondrial apoptosis in response to cardiac ischemia-reperfusion injury.Journal of translational medicine · 2025Review
- Protective effect of canagliflozin on post-resuscitation myocardial function in a rat model of cardiac arrest.Intensive care medicine experimental · 2023Article
- CBL knockdown protects cardiomyocytes against hypoxia-reoxygenation injury by downregulating GRB2 expression.Experimental and therapeutic medicine · 2022Article
- Genome-Wide Analysis Indicates a Complete Prostaglandin Pathway from Synthesis to Inactivation in Pacific White Shrimp,International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Post‑cardiac arrest myocardial dysfunction (PAMD) is a leading cause of death in patients undergoing resuscitation patients following cardiac arrest (CA). Although prostaglandin E1 (PGE1) is a clinical drug used to mitigate ischemia injury, its effect on PAMD remains unknown. In the present study, the protective effects of PGE1 on PAMD were evaluated in a rat model of CA and in a hypoxia‑reoxygenation (H/R)
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