ArticleMolecular and cellular biochemistry2004
Local delivery of soluble TNF-alpha receptor 1 gene reduces infarct size following ischemia/reperfusion injury in rats.
Article in Molecular and cellular biochemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 41 citations in OpenAlex.
- Soluble TNF receptors are associated with infarct size and ventricular dysfunction in ST-elevation myocardial infarction.PloS one · 2013Trial
- TNF-α, myocardial perfusion and function in patients with ST-segment elevation myocardial infarction and primary percutaneous coronary intervention.Clinical research in cardiology : official journal of the German Cardiac Society · 2012Trial
- The use of moderate hypothermia during cardiac surgery is associated with repression of tumour necrosis factor-alpha via inhibition of activating protein-1: an experimental study.Critical care (London, England) · 2006Trial
- Predictive Value of Adiponectin for Long-Term MACEs in Non-Diabetic STEMI Patients.Journal of clinical medicine · 2025Article
- Targeting neuro-immune systems to achieve cardiac tissue repair following myocardial infarction: A review of therapeutic approaches from in-vivo preclinical to clinical studies.Pharmacology & therapeutics · 2023Review
- Construction of miRNA-mRNA network reveals crucial miRNAs and genes in acute myocardial infarction.Journal of biomedical research · 2021Article
- Endoplasmic reticulum stress serves an important role in cardiac ischemia/reperfusion injury (Review).Experimental and therapeutic medicine · 2020Review
- 3,3'-Diindolylmethane protects cardiomyocytes from LPS-induced inflammatory response and apoptosis.BMC pharmacology & toxicology · 2018Article
- Protective Effects of Kaempferol against Myocardial Ischemia/Reperfusion Injury in Isolated Rat Heart via Antioxidant Activity and Inhibition of Glycogen Synthase Kinase-3β.Oxidative medicine and cellular longevity · 2015Article
- Disruption of group IVA cytosolic phospholipase A(2) attenuates myocardial ischemia-reperfusion injury partly through inhibition of TNF-α-mediated pathway.American journal of physiology. Heart and circulatory physiology · 2012Article
- Opioid receptor activation: suppression of ischemia/reperfusion-induced production of TNF-α in the retina.Investigative ophthalmology & visual science · 2011Article
- The extracellular matrix protein CCN1 dictates TNFα and FasL cytotoxicity in vivo.Advances in experimental medicine and biology · 2011Article
- AMPK and TNF-alpha at the crossroad of cell survival and death in ischaemic heart.Cardiovascular research · 2009Article
- Adiponectin protects against myocardial ischemia-reperfusion injury through AMPK- and COX-2-dependent mechanisms.Nature medicine · 2005Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis in the myocardium is linked to ischemia/reperfusion injury, and TNF-alpha induces apoptosis in cardiomyocytes. A significant amount of TNF-alpha is detected after ischemia and reperfusion. Soluble TNF-alpha receptor 1 (sTNFR1) is an extracellular domain of TNF-alpha receptor 1 and is an antagonist to TNF-alpha. In the present study, we examined the effects of sTNFR1 on infarct size in acute myocardial infarction (AMI) following ischemia/reperfusion. Male Wistar rats were subjected to left coronary artery (LCA) ligation. After 30 min of LCA occlusion, the temporary ligature on the LCA was released and blood flow was restored. Immediately after reperfusion, a total of 200 microg of sTNFR1 or LacZ plasmid was injected into three different sites of the left ventricular wall. At 6 h, 1 and 2 days after reperfusion, the TNF-alpha bioactivity in the myocardium was significantly higher in rats receiving LacZ plasmid than in sham-operated rats, whereas sTNFR1 plasmid significantly suppressed the increase in the TNF-alpha bioactivity. The sTNFR1 plasmid significantly reduced DNA fragmentation and caspase activity compared to the LacZ plasmid. Finally, the sTNFR1 expression-plasmid treatment significantly reduced the area of myocardial infarction at 2 days after ischemia/reperfusion compared to LacZ plasmid. In conclusion, the TNF-alpha bioactivity in the heart increased from the early stage of ischemia/reperfusion, and this increase was thought to contribute in part to the increased area of myocardial infarction. Suppression of TNF-alpha bioactivity with the sTNFR1 plasmid reduced the infarct size in AMI following ischemia and reperfusion.
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