ReviewFrontiers in physiology2018
ER-Mitochondria Microdomains in Cardiac Ischemia-Reperfusion Injury: A Fresh Perspective.
Review in Frontiers in physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.
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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.
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Who cites it
91 citing papers in PubMed.
- Intracellular Crosstalk of the Gasotransmitter Trio (NO, CO, HInternational journal of molecular sciences · 2026Review
- Review
- Insights in ischemia/reperfusion injury and cardioprotection: neglected and emerging pathways and therapeutic targets for a personalized therapy.Basic research in cardiology · 2026Review
- Nutritional Strategies and Aging: Current Evidence and Future Directions.Molecules (Basel, Switzerland) · 2026Review
- MAMs-Mediated Calcium Homeostasis in the Pathophysiology of Cardiovascular Diseases: A Mini-Review.Drug design, development and therapy · 2026Review
- Maternal High-Fat Diet Worsens Necrotizing Enterocolitis via Effects on Mitochondrial Function in Newborn Mice.Cellular and molecular gastroenterology and hepatology · 2026Article
- Targeting Mitochondria-Associated Endoplasmic Reticulum Membranes (MAMs): A Novel Therapeutic Strategy for Diabetic Complications.Diabetes, metabolic syndrome and obesity : targets and therapy · 2026Review
- High-intensity interval training improves mitochondrial function and attenuates cardiomyocytes damage in ischemia-reperfusion.International journal of cardiology. Heart & vasculature · 2025Review
- One Syndrome, Many Faces: A Unified Perspective on Heart Failure Phenotypes.International journal of molecular sciences · 2025Review
- Mitochondrial quality control as a therapeutic target in cardiovascular disease: Mechanistic insights and future directions.Journal of translational internal medicine · 2025Article
- Mitochondria-associated endoplasmic reticulum membranes and myocardial ischemia: from molecular mechanisms to therapeutic strategies.Journal of translational medicine · 2025Review
- Endoplasmic reticulum-mitochondria crosstalk: new mechanisms in the development of atherosclerosis.Frontiers in endocrinology · 2025Review
- Mitochondrial Dysfunction in Cardiac Disease: The Fort Fell.Biomolecules · 2024Review
- Hydrogen Protects Mitochondrial Function by Increasing the Expression of PGC-1α and Ameliorating Myocardial Ischaemia-Reperfusion Injury.Journal of cellular and molecular medicine · 2024Article
- Endoplasmic reticulum stress and mitochondrial dysfunction during aging: Role of sphingolipids.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2023Article
- Article
- Syntaxin 17 Protects Against Heart Failure Through Recruitment of CDK1 to Promote DRP1-Dependent Mitophagy.JACC. Basic to translational science · 2023Article
- Protective effects of Shen Yuan Dan on myocardial ischemia-reperfusion injury via the regulation of mitochondrial quality control.Cardiovascular diagnosis and therapy · 2023Article
- Aging Hallmarks and the Role of Oxidative Stress.Antioxidants (Basel, Switzerland) · 2023Review
- Inflammation and Heart Failure: Searching for the Enemy-Reaching the Entelechy.Journal of cardiovascular development and disease · 2023Review
31 more citing papers are in PubMed but not listed here.
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
The mitochondrial and endoplasmic reticulum (ER) homeostasis is pivotal to the maintenance of an array of physiological processes. The physical contact and association between ER and mitochondria, known as the ER-mitochondria microdomains or mitochondria-associated ER membrane (MAM), temporally and spatially regulates the mitochondria/ER structure and function. More evidence suggests a role for MAMs in energy production, cellular contraction and mobility, and normal extracellular signal transmission. In pathological states, such as cardiac ischemia-reperfusion (I/R injury), this ER-mitochondria microdomains may act to participate in the cellular redox imbalance, ER stress, mitochondrial injury, energy deletion, and programmed cell death. From a therapeutic perspective, a better understanding of the cellular and molecular mechanisms of the pathogenic ER-mitochondria contact should help to identify potential therapeutic target for cardiac I/R injury and other cardiovascular diseases and also pave the road to new treatment modalities pertinent for the treatment of reperfusion damage in clinical practice. This review will mainly focus on the possible signaling pathways involved in the regulation of the ER-mitochondria contact. In particular, we will summarize the downstream signaling modalities influenced by ER-mitochondria microdomains, for example, mitochondrial fission, mitophagy, calcium balance, oxidative stress, and programmed cell death in details.
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