Effective Agents Targeting the Mitochondria and Apoptosis to Protect the Heart
A wide variety of agents have been traditionally used in cardiovascular medicine worldwide and their precise mechanisms of action have been demonstrated to be largely related to the cardiomyocyte mitochondria and apoptosis. Abnormalities in the structure and function of the mitochondria and mutations in mitochondrial DNA can decrease energy production, alter the redox system, impair calcium homeostasis, and induce the mitochondrial permeability transition pore (MPTP), causing cell death. All of these data provide evidence of mitochondrial signaling pathways as targets to downregulate cardiac cell apoptosis and thus to prevent and treat cardiovascular diseases. This review focuses on the protective roles of various agents, mostly natural compounds, which express beneficial effects on mitochondrial function and suspend the apoptotic signaling mechanisms by modulating the activity of mitogen-activated protein kinases (MAPKs). Examining cellular and molecular targets of these agents offers essential experimental information for future pharmacological studies, drug discovery, clinical trials and applications.
No Supplementary Data
No Article Media
Document Type: Research Article
Publication date: March 1, 2017
More about this publication?
- Current Pharmaceutical Design publishes timely in-depth reviews covering all aspects of current research in rational drug design. Each issue is devoted to a single major therapeutic area. A Guest Editor who is an acknowledged authority in a therapeutic field has solicits for each issue comprehensive and timely reviews from leading researchers in the pharmaceutical industry and academia.
Each thematic issue of Current Pharmaceutical Design covers all subject areas of major importance to modern drug design, including: medicinal chemistry, pharmacology, drug targets and disease mechanism.
- Editorial Board
- Information for Authors
- Subscribe to this Title
- Ingenta Connect is not responsible for the content or availability of external websites