Stress-activated MAP kinases in cardiac remodeling and heart failure; new insights from transgenic studies.
Activation of stress-activated mitogen-activated protein kinases (SAPKs), mainly c-Jun N-terminal kinase (JNK) and p38, have long been associated with different forms of cardiac pathology across a wide spectrum of species. However, their specific roles in the development of heart failure are still unclear. Previous studies in neonatal myocytes in culture suggest a critical role for both JNK and p38 in hypertrophy and apoptosis. A far more complex picture has been provided by recent observations from both cellular and transgenic models that have not only challenged their role in hypertrophy and cell death but have also pointed out novel functions of SAPKs in different aspects of cardiac pathology, including contractile function, extracellular matrix remodeling, intercellular communication, and metabolic regulation.
Petrich
Brian G
BG
Division of Molecular Medicine, Departments of Anesthesiology and Medicine, University of California at Los Angeles, Los Angeles, California 90095, USA.
Wang
Yibin
Y
D000818:Animals; D030801:Animals, Genetically Modified; D017209:Apoptosis / Q000502:physiology; D006332:Cardiomegaly / Q000201:enzymology; D006333:Heart Failure / Q000201:enzymology* / Q000209:etiology; D006801:Humans; D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D023421:Models, Animal; D009200:Myocardial Contraction / Q000502:physiology; D013312:Stress, Physiological / Q000150:complications / Q000201:enzymology*; D020257:Ventricular Remodeling / Q000502:physiology; D048051:p38 Mitogen-Activated Protein Kinases
D048031:JNK Mitogen-Activated Protein Kinases; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases