PPARδ, a Potential Therapeutic Target for Heart Disease

Figures

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  Figure 1:. PPARδ plays a crucial role in cardiac pathophysiology: PPARδ signaling is impaired in the heart under various pathological conditions, such as pathological cardiac hypertrophy, myocardial ischemia/reperfusion, doxorubicin cardiotoxicity and diabetic cardiomyopathy. PPARδ deficiency in the heart leads to cardiac dysfunction, myocardial lipid accumulation, cardiac hypertrophy/remodeling and heart failure.

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  Figure 2:. The pleiotropic and integrated effects of PPARδ that affects cardiac structure and function. Investigations in the past 15 years uncovered the potential mechanisms underlying the beneficial roles of cardiac PPARδ in determining cardiac pathophysiology. In addition to direct transcription regulation of mitochondrial biogenesis, substrate utilization and antioxidant defense in the heart, PPARδ exerts anti-inflammation and cardiomyocyte proliferated effects probably via interacting with other transcription factors and cellular signaling pathways.

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  Figure 3:. Upstream regulation of PPARδ in the heart. The cardiac expression and activity of PPARδ can be elevated by various PPARδ agonists (endogenous, synthetic and natural ligands), post-translational modification (deSUMOylation), leptin and AMPK (AMP-activated protein kinase). In contrast, PPARδ antagonists, microRNA (miR-199a-214) and nuclear receptor coregulator (Nuclear receptor coactivator 6). Arrows with solid lines: activation; Arrows with dash lines: inhibition.