Gp130-mediated pathway and left ventricular remodeling.
The binding of ligands to gp130 activates the JAK/STAT pathway, where STAT3 plays a central role in transmitting signals from the membrane to the nucleus. Cardiac-specific disruption of gp130 was shown to present heart failure in response to mechanical stress accompanied by an increase in apoptosis. Thus, the inactivation of STAT3 resulting from the loss of gp130 may be a key event in the transition from cardiac hypertrophy to heart failure. Vascular formation mediated by VEGF is known to be an essential in the maintenance of cardiac function. In this review, STAT3 is highlighted as a regulator of antiogenic factors, and together with bclxL and MnSOD, promotes cardiac myocyte survival by prevention of apoptosis and restoration of energy deprivation. Cytoprotective signal through gp130 would provide new insight into the pathophysiologic significance of cytokines in the process of cardiac remodeling.
Yamauchi-Takihara
Keiko
K
Department of Molecular Medicine, Osaka University Graduate School of Medicine, Osaka, Japan.
D000818:Animals; D015703:Antigens, CD / Q000502:physiology*; D050822:Cytokine Receptor gp130; D004268:DNA-Binding Proteins / Q000502:physiology; D006801:Humans; D017379:Hypertrophy, Left Ventricular; D008562:Membrane Glycoproteins / Q000502:physiology*; D050796:STAT3 Transcription Factor; D015398:Signal Transduction; D015534:Trans-Activators / Q000502:physiology; D020257:Ventricular Remodeling
D015703:Antigens, CD; D004268:DNA-Binding Proteins; C494199:IL6ST protein, human; D008562:Membrane Glycoproteins; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; D015534:Trans-Activators; D050822:Cytokine Receptor gp130