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.
Highlights
Anti-Fibrotic Effects of Curcumin and Some of its Analogues in the Heart Armita Mahdavi Gorabi; Saeideh Hajighasemi; Nasim Kiaie; Giuseppe M
This study demonstrated that Cur administration attenuates cardiac fibroblasts (CFs) proliferation and migration and keeps their collagen production at baseline level regardless of the presence of Transforming growth factor β1 (TGF-β1) or Ang II [57]
GW9662 pre-treatment, on the other hand, exerted negative effects on Cur-induced antifibrotic activities [13] suggesting that Cur can suppress the cardiac fibrosis in SHRs via modulating Peroxisome proliferator-activated receptor-γ (PPAR-γ) and TGF-β1/Smad2/3 signaling interaction [13]
Summary
Cardiac fibrosis condition induced by Combined aortic regurgitation and aortic stenosis Myocardial infarction (MI). TGF-β administration -High glucose (HG) -Streptozotocin (STZ) injection (diabetes induction). -Upregulation of MMP-2 - Upregulation of MMP-9 -Reduction of collagen deposition -Decreased perivascular fibrosis expansion -Additive effect on fibrosis extent when combined with enalapril -Repressed expression of p300 transcriptional coactivator observed only in animals subjected to enalapril+Cur -Blunted PAI-1 protein level. - PKC-α inactivation -PKC-β2 inactivation -Phosphorylation diminution of p38MAPK and ERK1/2 -Downregulation of TGF- β, osteopontin and p300 -Attenuated ECM accumulation - Reduced TLR2 expression - Lowered macrophage infiltration (CD68) and high
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