Journal
ARCHIVES OF PHARMACAL RESEARCH
Volume 39, Issue 8, Pages 1100-1113Publisher
PHARMACEUTICAL SOC KOREA
DOI: 10.1007/s12272-016-0809-6
Keywords
Myofibroblasts; Inflammation; Myocardial infarction; Cardiac fibrosis; Signaling molecules
Categories
Funding
- National Science and Technology Development Agency (NSTDA) [P-12-01409]
- Center of Excellence for Innovation in Drug Design and Discovery, Faculty of Pharmacy, Mahidol University
- JSPS KAKENHI [25253011]
- Uehara Memorial Foundation
- Grants-in-Aid for Scientific Research [25253011] Funding Source: KAKEN
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On myocardial infarction, many cells are injured or died owing to arterial occlusion. Intracellular molecules released from injured or dead cells initiate inflammatory responses that play important roles in cardiac remodeling including fibrosis. Fibrosis is an excess accumulation of extracellular collagen. Currently, drugs used to treat cardiac fibrosis are not commercially available. Myofibroblasts are responsible for the production and secretion of collagen. Infiltrating inflammatory cells interact with fibroblasts or other cells and promote myofibroblast formation. Inflammatory cells also modulate the activities of myofibroblasts. Regulation of collagen production is critical for modulating the progression of fibrosis. Hence, the manipulation of activities of inflammatory cells and myofibroblasts will provide promising therapeutic targets for treatment of cardiac fibrosis.
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