ArticleThe Journal of pharmacology and experimental therapeutics2011
Chymase inhibition reduces infarction and matrix metalloproteinase-9 activation and attenuates inflammation and fibrosis after acute myocardial ischemia/reperfusion.
Article in The Journal of pharmacology and experimental therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 88 citations in OpenAlex.
- Shenqi Granules Enhance Recovery from Myocardial Ischemia-Reperfusion Injury by Downregulating MMP9 and ADH1C.Pharmaceuticals (Basel, Switzerland) · 2026Article
- N-terminal domain of CTRP9 promotes cardiac fibroblast activation in myocardial infarction via Rap1/Mek/Erk pathway.Journal of translational medicine · 2025Article
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- Mast cells: a novel therapeutic avenue for cardiovascular diseases?Cardiovascular research · 2024Review
- Mast Cells in Cardiac Remodeling: Focus on the Right Ventricle.Journal of cardiovascular development and disease · 2024Review
- Cardiac fibrogenesis: an immuno-metabolic perspective.Frontiers in physiology · 2024Review
- Tryptase and Exogenous Trypsin: Mechanisms and Ophthalmic Applications.Journal of inflammation research · 2023Review
- Impact of early pericardial fluid chymase activation after cardiac surgery.Frontiers in cardiovascular medicine · 2023Article
- Pathophysiological Role of Chymase-Activated Matrix Metalloproteinase-9.Biomedicines · 2022Review
- Histamine receptors in heart failure.Heart failure reviews · 2022Review
- Effects of Neonatal Administration of Non-Opiate Analogues of Leu-Enkephalin to Heart Tissue Homeostasis of Prepubertal Albino Rats Exposed to Hypoxia.Bulletin of experimental biology and medicine · 2022Article
- Commentary: If it looks too good to be true, it probably is.JTCVS techniques · 2021Article
- Post-Ischemic Treatment of Recombinant Human Secretory Leukocyte Protease Inhibitor (rhSLPI) Reduced Myocardial Ischemia/Reperfusion Injury.Biomedicines · 2021Article
- The Impact of the Renin-Angiotensin-Aldosterone System on Inflammation, Coagulation, and Atherothrombotic Complications, and to Aggravated COVID-19.Frontiers in pharmacology · 2021Review
- A novel serine protease inhibitor as potential treatment for dry eye syndrome and ocular inflammation.Scientific reports · 2020Article
- Novel Insight into the in vivo Function of Mast Cell Chymase: Lessons from Knockouts and Inhibitors.Journal of innate immunity · 2020Review
- Increase of chymase-dependent angiotensin II-forming activity in circulating mononuclear leukocytes after acute myocardial infarction chymase activity after acute myocardial infarction.Heart and vessels · 2019Observational
- Sex differences in gene expression in response to ischemia in the human left ventricular myocardium.Human molecular genetics · 2019Article
- A Chymase Inhibitory RNA Aptamer Improves Cardiac Function and Survival after Myocardial Infarction.Molecular therapy. Nucleic acids · 2019Article
- Japanese encephalitis virus neuropenetrance is driven by mast cell chymase.Nature communications · 2019Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Chymase is activated after acute myocardial ischemia/reperfusion (AMI-R) and is associated with an early activation of matrix metalloproteinase-9 (MMP-9), which increases infarct size after experimental AMI, and late fibrosis. We assessed the effect of chymase inhibition on myocardial protection and early signs of fibrosis after AMI-R. Fourteen pigs underwent AMI-R and received intravenously either vehicle (V; n = 7) or chymase inhibitor (CM; n = 7). Separately, rat myocardial fibroblast was incubated with vehicle (n = 4), low-dose chymase (n = 4), high-dose chymase (n = 4), or high-dose chymase plus chymase inhibitor (n = 4). Infarct size (V, 41 ± 5; CM, 24 ± 5; P < 0.01) and serum troponin T (P = 0.03) at the end of reperfusion were significantly reduced in CM. Chymase activity in both the area at risk (AAR) (P = 0.01) and nonischemic area (P = 0.02) was significantly lower in CM. Myocardial levels of pro, cleaved, and cleaved/pro-MMP-9 in the AAR were significantly lower in CM than V (P < 0.01, < 0.01, and = 0.02, respectively), whereas phospho-endothelial nitric-oxide synthase (eNOS) (P < 0.01) and total eNOS (P = 0.03) were significantly higher in CM. Apoptotic cells (P = 0.05), neutrophils (P < 0.05), and MMP-9-colocalizing mast cells (P < 0.05) in the AAR were significantly reduced in CM. Interleukin-18 (P < 0.05) and intercellular adhesion molecule-1 (P < 0.05) mRNA levels were significantly lower in CM. In cultured cardiac fibrosis, Ki-67-positive cells were significantly higher in the high-dose chymase groups (P < 0.03). This study demonstrates that chymase inhibition plays crucial roles in myocardial protection related to MMP-9, inflammatory markers, and the eNOS pathway. It may also attenuate fibrosis induced by activated chymase after AMI-R.
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