ArticleJournal of the American Heart Association2017
Targeting of Extracellular RNA Reduces Edema Formation and Infarct Size and Improves Survival After Myocardial Infarction in Mice.
Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.
- Non-coding RNAs modulate autophagy in myocardial ischemia-reperfusion injury: a systematic review.Journal of cardiothoracic surgery · 2021Pooled it
- Plasma Circulating Extracellular RNAs in Left Ventricular Remodeling Post-Myocardial Infarction.EBioMedicine · 2018Trial
- Extracellular RNA as a molecular driver and therapeutic target in abdominal aortic aneurysms.Scientific reports · 2025Article
- MK2 deficiency decreases mortality in male mice during the inflammatory phase after myocardial infarction.Physiological reports · 2025Article
- Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2024Review
- Recent advances in the diagnosis and management of acute myocardial infarction.Journal of the Chinese Medical Association : JCMA · 2023Review
- Article
- Early DNase-I therapy delays secondary brain damage after traumatic brain injury in adult mice.Scientific reports · 2023Article
- The ebb and flow of cardiac lymphatics: a tidal wave of new discoveries.Physiological reviews · 2023Review
- CD69 expression on regulatory T cells protects from immune damage after myocardial infarction.The Journal of clinical investigation · 2022Article
- Emerging biological functions of ribonuclease 1 and angiogenin.Critical reviews in biochemistry and molecular biology · 2022Review
- Ribonuclease-1 treatment after traumatic brain injury preserves blood-brain barrier integrity and delays secondary brain damage in mice.Scientific reports · 2022Article
- Self-extracellular RNA promotes pro-inflammatory response of astrocytes to exogenous and endogenous danger signals.Journal of neuroinflammation · 2021Article
- Targeting Inflammation After Myocardial Infarction.Current cardiology reports · 2020Review
- Ribonuclease 1 attenuates septic cardiomyopathy and cardiac apoptosis in a murine model of polymicrobial sepsis.JCI insight · 2020Article
- Extracellular nucleic acid scavenging rescues rats from sulfur mustard analog-induced lung injury and mortality.Archives of toxicology · 2020Article
- Extracellular RNA as a Versatile DAMP and Alarm Signal That Influences Leukocyte Recruitment in Inflammation and Infection.Frontiers in cell and developmental biology · 2020Review
- Endothelial Ribonuclease 1 in Cardiovascular and Systemic Inflammation.Frontiers in cell and developmental biology · 2020Review
- The Extraordinary Role of Extracellular RNA in Arteriogenesis, the Growth of Collateral Arteries.International journal of molecular sciences · 2019Review
- Extracellular RNA in Central Nervous System Pathologies.Frontiers in molecular neuroscience · 2019Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFollowing myocardial infarction (MI), peri-infarct myocardial edema formation further impairs cardiac function. Extracellular RNA (eRNA) released from injured cells strongly increases vascular permeability. This study aimed to assess the role of eRNA in MI-induced cardiac edema formation, infarct size, cardiac function, and survival after acute MI and to evaluate the therapeutic potential of ribonuclease 1 (RNase-1) treatment as an eRNA-degrading intervention. METHODS AND
resultsC57BL/6J mice were subjected to MI by permanent ligation of the left anterior descending coronary artery. Plasma eRNA levels were significantly increased compared with those in controls starting from 30 minutes after ligation. Systemic application of RNase-1, but not DNase, significantly reduced myocardial edema formation 24 hours after ligation compared with controls. Consequently, eRNA degradation by RNase-1 significantly improved the perfusion of collateral arteries in the border zone of the infarcted myocardium 24 hours after ligation of the left anterior descending coronary artery, as detected by micro-computed tomography imaging. Although there was no significant difference in the area at risk, the area of vital myocardium was markedly larger in mice treated with RNase-1 compared with controls, as detected by Evans blue and 2,3,5-triphenyltetrazolium chloride staining. The increase in viable myocardium was associated with significantly preserved left ventricular function, as assessed by echocardiography. Moreover, RNase-1 significantly improved 8-week survival following MI.
conclusionseRNA is an unrecognized permeability factor in vivo, associated with myocardial edema formation after acute MI. RNase-1 counteracts eRNA-induced edema formation and preserves perfusion of the infarction border zone, reducing infarct size and protecting cardiac function after MI.
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Registered trials
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