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Role of osteopontin in heart failure associated with aging
Mahipal Singh1, Cerrone R Foster, Suman Dalal
1Department of Physiology, James H Quillen College of Medicine, East Tennessee State University, PO Box 70576, Johnson City, TN 37614, USA.
Insights
Osteopontin (OPN) expression increases in the heart after myocardial infarction (MI). Increased OPN shows a protective role in healing post-MI, modulating cardiac remodeling and fibrosis.
Area of Science:
- Cardiovascular Biology
- Regenerative Medicine
- Aging Research
Background:
- Cardiovascular disease is a primary cause of death in the elderly, with acute ischemic events like myocardial infarction (MI) leading to significant morbidity and mortality.
- Aging exacerbates adverse cardiac remodeling post-MI, characterized by impaired repair, infarct expansion, and septal hypertrophy.
- Osteopontin (OPN) expression is upregulated in the heart following MI, suggesting a potential role in cardiac response.
Purpose of the Study:
- To review the expression of osteopontin (OPN) in the heart after myocardial infarction (MI).
- To elucidate the role of OPN in the different phases of cardiac infarct healing.
- To explore OPN's influence on molecular and cellular changes during post-MI recovery.
Main Methods:
- Literature review focusing on studies investigating OPN expression and function post-MI.
- Analysis of evidence from transgenic mouse models regarding OPN's impact on left ventricular (LV) remodeling.
- Examination of OPN's role in the inflammatory, repair, and remodeling phases of infarct healing.
Main Results:
- Increased OPN expression post-MI suggests a protective function in cardiac remodeling.
- OPN modulates collagen deposition and fibrosis, crucial processes in scar formation and tissue repair.
- Studies indicate OPN influences key cellular events including inflammation, fibroblast activity, and angiogenesis during infarct healing.
Conclusions:
- Osteopontin (OPN) plays a significant role in modulating the cardiac response to myocardial infarction (MI).
- OPN's protective effects on post-MI left ventricular remodeling are linked to its influence on fibrosis and extracellular matrix deposition.
- Understanding OPN's function in infarct healing offers potential therapeutic targets for improving outcomes in elderly patients with cardiovascular disease.
Abstract:
Cardiovascular disease is one of the leading causes of death in the elderly. Much of the morbidity and mortality in the elderly is attributable to acute ischemic events leading to myocardial infarction (MI) and death of cardiac myocytes. Evidence has been provided that aging associated with adverse remodeling post MI as demonstrated by less effective myocardial repair, greater infarct expansion, and septal hypertrophy. Expression of osteopontin (OPN) increases in the heart post MI. Transgenic mice studies suggest that increased expression of OPN plays a protective role in post-MI LV remodeling by modulating collagen deposition and fibrosis. OPN, a multifunctional protein, has the potential to influence the molecular and cellular changes associated with infarct healing. The post-MI infarct healing process involves temporarily overlapping phases that include the following--(1) inflammation with migration and adhesion of neutrophils and macrophages, phagocytosis and inflammatory gene expression; (2) tissue repair with fibroblast adhesion and proliferation, myofibroblast differentiation, extracellular matrix deposition and scar formation; and (3) structural and functional remodeling of infarcted and non-infarcted myocardium through cardiac myocyte apoptosis, hypertrophy and myocardial angiogenesis. This review is focused on the expression of OPN in the heart post MI and its role in various phases of infarct healing.
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