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Malonate given at reperfusion prevents post-myocardial infarction heart failure by decreasing ischemia/reperfusion injury

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Title: Malonate given at reperfusion prevents post-myocardial infarction heart failure by decreasing ischemia/reperfusion injury
Authors: Jiro Abe, Ana Vujic, Hiran A. Prag, Michael P. Murphy, Thomas Krieg
Contributors: DSpace at Cambridge pro (8.1)
Source: Basic Res Cardiol
Abe, J, Vujic, A, Prag, H A, Murphy, M P & Krieg, T 2024, 'Malonate given at reperfusion prevents post-myocardial infarction heart failure by decreasing ischemia/reperfusion injury', Basic Research in Cardiology, vol. 119, no. 4, pp. 691-697. https://doi.org/10.1007/s00395-024-01063-z
Publisher Information: Springer Science and Business Media LLC, 2024.
Publication Year: 2024
Subject Terms: Male, Succinate, Time Factors, Myocardium/metabolism, Malonates/pharmacology, Myocardial Infarction, Myocardial Reperfusion Injury/prevention & control, Myocardial Reperfusion Injury, Ischemia/reperfusion injury, Inbred C57BL, Left/drug effects, Ventricular Function, Left, Heart Failure/prevention & control, Mice, Ventricular Function, Animals, Ventricular Function, Left/drug effects, Myocytes, Cardiac, Myocardial Infarction/metabolism, Heart Failure, Myocytes, Animal, Myocardium, Malonate, Myocytes, Cardiac/metabolism, Original Contribution, Heart failure with reduced ejection fraction, Fibrosis, Malonates, Mitochondria, 3. Good health, Mice, Inbred C57BL, Disease Models, Animal, Disease Models, Cardiac/metabolism, Reactive oxygen species
Description: The mitochondrial metabolite succinate is a key driver of ischemia/reperfusion injury (IRI). Targeting succinate metabolism by inhibiting succinate dehydrogenase (SDH) upon reperfusion using malonate is an effective therapeutic strategy to achieve cardioprotection in the short term ( 60%) and fractional shortening (~ 30%), as well as significantly less collagen deposition than control hearts. Malonate administration upon reperfusion prevents post-MI HF. Acidification of malonate enables lower doses of malonate to also achieve long-term cardioprotection post-MI. Therefore, the administration of acidified malonate upon reperfusion is a promising therapeutic strategy to prevent IRI and post-MI HF.
Document Type: Article
Other literature type
File Description: application/pdf; text/xml
Language: English
ISSN: 1435-1803
DOI: 10.1007/s00395-024-01063-z
Access URL: https://pubmed.ncbi.nlm.nih.gov/38864895
https://research.manchester.ac.uk/en/publications/d148d01d-bbfc-44ee-99d9-97a7a64024b4
https://doi.org/10.1007/s00395-024-01063-z
https://www.repository.cam.ac.uk/handle/1810/372727
https://doi.org/10.1007/s00395-024-01063-z
https://www.repository.cam.ac.uk/handle/1810/369563
https://doi.org/10.1007/s00395-024-01063-z
Rights: CC BY
Accession Number: edsair.doi.dedup.....b0b4c0c7c5a5dd41086c0b505347e7c1
Database: OpenAIRE
Description
Abstract:The mitochondrial metabolite succinate is a key driver of ischemia/reperfusion injury (IRI). Targeting succinate metabolism by inhibiting succinate dehydrogenase (SDH) upon reperfusion using malonate is an effective therapeutic strategy to achieve cardioprotection in the short term ( 60%) and fractional shortening (~ 30%), as well as significantly less collagen deposition than control hearts. Malonate administration upon reperfusion prevents post-MI HF. Acidification of malonate enables lower doses of malonate to also achieve long-term cardioprotection post-MI. Therefore, the administration of acidified malonate upon reperfusion is a promising therapeutic strategy to prevent IRI and post-MI HF.
ISSN:14351803
DOI:10.1007/s00395-024-01063-z