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Myocardial infarction (MI) is still a global illness with a high morbidity and death rate, despite significant advancements in therapy. Even though there is a cure for myocardial infarction treatment, novel therapeutic strategies for cardioprotection and cardiac repair are beginning to emerge. Evidence of pathological features in MI demonstrates cell signalling pathways involved in cardiomyocyte, endothelial cell, fibroblast, monocyte, and stem cell survival, proliferation, apoptosis, and autophagy. The signalling pathways plays major in all the pathological features. The major players in oxidative stress and apoptosis, such as Notch, Nrf2/HO-1 pathways and the main regulator of angiogenesis, MAPK, JAK/STAT pathways. These signalling pathways plays an important role in the pathogenesis of MI and targeting these pathways improves the pathological symptoms which is promising. The most widely used method for inducing MI in animal is isoproterenol induced myocardial infarction. It is non-invasive, rapid, simple method for producing myocardial damage in animal that is like MI seen in humans. In this review, we summarize the signalling pathways involved in myocardial infarction and the treatment approaches for MI by controlling these related pathways, which help to restore and reestablish injured hearts by reducing inflammation, preventing cardiomyocyte death, and promoting angiogenesis and the molecular mechanism involved in isoproterenol induced myocardial infarction.
Keywords:
Signalling pathways, MI – Myocardial Infarction, ISO – Isoproterenol
Cite Article:
"Signalling Pathways in Myocardial Infarction: Drug Therapeutic Strategies and Molecular Insights into Isoproterenol-Induced Cardiac Damage", International Journal of Science & Engineering Development Research (www.ijrti.org), ISSN:2455-2631, Vol.9, Issue 3, page no.726 - 741, March-2024, Available :http://www.ijrti.org/papers/IJRTI2403100.pdf
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000205142
ISSN:
2456-3315 | IMPACT FACTOR: 8.14 Calculated By Google Scholar| ESTD YEAR: 2016
An International Scholarly Open Access Journal, Peer-Reviewed, Refereed Journal Impact Factor 8.14 Calculate by Google Scholar and Semantic Scholar | AI-Powered Research Tool, Multidisciplinary, Monthly, Multilanguage Journal Indexing in All Major Database & Metadata, Citation Generator