Abstract
Chronic heart failure is debilitating, often fatal, expensive to treat and common. In most patients it is a late consequence of myocardial infarction (MI). The intracellular signals following infarction that lead to diminished contractility, apoptosis, fibrosis and ultimately heart failure are not fully understood but probably involve p38-mitogen activated protein kinases (p38), a family of serine/threonine kinases which, when activated, cause cardiomyocyte contractile dysfunction and death. Pharmacological inhibitors of p38 suppress inflammation and are undergoing clinical trials in rheumatoid arthritis, Chrohn's disease, psoriasis and surgery-induced tissue injury. In this review, we discuss the mechanisms, circumstances and consequences of p38 activation in the heart. The purpose is to evaluate p38 inhibition as a potential therapy for ischaemic heart disease. (c) 2007 Elsevier Inc. All rights reserved
| Original language | English |
|---|---|
| Pages (from-to) | 192 - 206 |
| Number of pages | 15 |
| Journal | Pharmacology and Therapeutics |
| Volume | 116 |
| Issue number | 2 |
| Publication status | Published - Nov 2007 |