ReviewMolecular and cellular biochemistry2005
Apoptosis and oncosis in acute coronary syndromes: assessment and implications.
Review in Molecular and cellular biochemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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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.
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.
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Who cites it
14 citing papers in PubMed, 51 citations in OpenAlex.
- Early markers of myocardial ischemia: from the experimental model to forensic pathology cases of sudden cardiac death.International journal of legal medicine · 2018Observational
- Early markers for myocardial ischemia and sudden cardiac death.International journal of legal medicine · 2016Article
- Intervention timing and effect of PJ34 on astrocytes during oxygen-glucose deprivation/reperfusion and cell death pathways.Journal of Huazhong University of Science and Technology. Medical sciences = Hua zhong ke ji da xue xue bao. Yi xue Ying De wen ban = Huazhong keji daxue xuebao. Yixue Yingdewen ban · 2015Article
- Proteomic analysis of apoptotic and oncotic pancreatic acinar AR42J cells treated with caerulein.Molecular and cellular biochemistry · 2013Article
- The impact of pressure overload on coronary vascular changes following myocardial infarction in rats.American journal of physiology. Heart and circulatory physiology · 2013Article
- In situ ligation: a decade and a half of experience.Methods in molecular biology (Clifton, N.J.) · 2011Review
- Sevoflurane postconditioning prevents activation of caspase 3 and 9 through antiapoptotic signaling after myocardial ischemia-reperfusion.Journal of anesthesia · 2010Article
- Blockade of Hsp20 phosphorylation exacerbates cardiac ischemia/reperfusion injury by suppressed autophagy and increased cell death.Circulation research · 2009Article
- Role of healing-specific-matricellular proteins and matrix metalloproteinases in age-related enhanced early remodeling after reperfused STEMI in dogs.Molecular and cellular biochemistry · 2009Article
- Ultrastructural definition of apoptosis in heart failure.Heart failure reviews · 2008Review
- Induction of apoptosis by artemisinin relieving the severity of inflammation in caerulein-induced acute pancreatitis.World journal of gastroenterology · 2007Article
- Impaired perfusion after myocardial infarction is due to reperfusion-induced deltaPKC-mediated myocardial damage.Cardiovascular research · 2007Article
- Immunohistochemical expression of activated caspase-3 in human myocardial infarction.Virchows Archiv : an international journal of pathology · 2006Article
- Rho kinase in the regulation of cell death and survival.Archivum immunologiae et therapiae experimentalisReview
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The rational design of therapeutic interventions for protection of ischemic myocardium from ultimate death requires an understanding of the mechanistic basis of cardiomyocyte (CM) cell death, its timing and the tools for its quantification. Until recently, CM cell death following ischemia and/or reperfusion was considered to involve necrosis or 'accidental cell death' from very early on. Collective evidence over the past decade indicates that early CM cell death after myocardial ischemia and post-ischemic reperfusion involves apoptosis with cell shrinkage and drop-out, and/or oncosis with cell swelling followed by necrosis. This paradigm shift suggests that different approaches for cardioprotection are required. Oncologists, pathologists, anatomists and basic scientists who have studied apoptosis over the last three decades separated physiological apoptosis from inappropriate apoptosis in pathological states. Until recently, cardiologists resisted the concepts of CM apoptosis and regeneration. Cumulative evidence indicating that apoptosis in the heart may occur in different cell types, spread from one cell type to another, and occur in bursts, may have profound implications for therapies aimed at protection of ischemic myocardium by targeting CM apoptosis in acute coronary syndromes. This review focuses on a critique of the methods used for the assessment of CM apoptosis and the implications of CM apoptosis in acute coronary syndromes.
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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.