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Heart Fail Rev. 2019 Sep 11. doi: 10.1007/s10741-019-09854-6. [Epub ahead of print]

Anti-fibrotic effects of curcumin and some of its analogues in the heart.

Author information

1
Research Center for Advanced Technologies in Cardiovascular Medicine, Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran.
2
Department of Medical Biotechnology, Faculty of Paramedicine, Qazvin University of Medical Sciences, Qazvin, Iran.
3
Department of Medical Sciences, IRCCS San Raffaele Roma, Rome, Italy.
4
Department of Academic Diabetes, Endocrinology and Metabolism, Hull York Medical School, University of Hull, Hull, UK.
5
Medical Research Centre, Sultan Qaboos University, Muscat, Oman.
6
Department of Biochemistry, College of Medicine and Health Sciences, Sultan Qaboos University, Muscat, Oman.
7
Neurogenic Inflammation Research Center, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir.
8
Biotechnology Research Center, Pharmaceutical Technology Institute, Mashhad University of Medical Sciences, Mashhad, 9177948564, Iran. sahebkara@mums.ac.ir.
9
School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran. sahebkara@mums.ac.ir.

Abstract

Cardiac fibrosis stems from the changes in the expression of fibrotic genes in cardiac fibroblasts (CFs) in response to the tissue damage induced by various cardiovascular diseases (CVDs) leading to their transformation into active myofibroblasts, which produce high amounts of extracellular matrix (ECM) proteins leading, in turn, to excessive deposition of ECM in cardiac tissue. The excessive accumulation of ECM elements causes heart stiffness, tissue scarring, electrical conduction disruption and finally cardiac dysfunction and heart failure. Curcumin (Cur; also known as diferuloylmethane) is a polyphenol compound extracted from rhizomes of Curcuma longa with an influence on an extensive spectrum of biological phenomena including cell proliferation, differentiation, inflammation, pathogenesis, chemoprevention, apoptosis, angiogenesis and cardiac pathological changes. Cumulative evidence has suggested a beneficial role for Cur in improving disrupted cardiac function developed by cardiac fibrosis by establishing a balance between degradation and synthesis of ECM components. There are various molecular mechanisms contributing to the development of cardiac fibrosis. We presented a review of Cur effects on cardiac fibrosis and the discovered underlying mechanisms by them Cur interact to establish its cardio-protective effects.

KEYWORDS:

C66; Cardiac fibrosis; Curcumin; Diferuloylmethane; J19

PMID:
31512150
DOI:
10.1007/s10741-019-09854-6

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