ArticleCardiovascular research2011
Cardiac-specific mindin overexpression attenuates cardiac hypertrophy via blocking AKT/GSK3β and TGF-β1-Smad signalling.
Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 84 citations in OpenAlex.
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- Transforming growth factor-β and bone morphogenetic protein signaling pathways in pathological cardiac hypertrophy.Cell cycle (Georgetown, Tex.) · 2023Review
- TRAF Family Member 4 Promotes Cardiac Hypertrophy Through the Activation of the AKT Pathway.Journal of the American Heart Association · 2023Article
- Tisp40 prevents cardiac ischemia/reperfusion injury through the hexosamine biosynthetic pathway in male mice.Nature communications · 2023Article
- OSMR deficiency aggravates pressure overload-induced cardiac hypertrophy by modulating macrophages and OSM/LIFR/STAT3 signalling.Journal of translational medicine · 2023Article
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- Endothelial ERG alleviates cardiac fibrosis via blocking endothelin-1-dependent paracrine mechanism.Cell biology and toxicology · 2021Article
- Fibronectin type III domain-containing 5 in cardiovascular and metabolic diseases: a promising biomarker and therapeutic target.Acta pharmacologica Sinica · 2021Article
- Matrine attenuates pathological cardiac fibrosis via RPS5/p38 in mice.Acta pharmacologica Sinica · 2021Article
- Therapeutic miR-21 Silencing Reduces Cardiac Fibrosis and Modulates Inflammatory Response in Chronic Chagas Disease.International journal of molecular sciences · 2021Article
- Article
- Qindan Capsule Attenuates Myocardial Hypertrophy and Fibrosis in Pressure Overload-Induced Mice Involving mTOR and TGF-Evidence-based complementary and alternative medicine : eCAM · 2021Article
- Anti-Myocardial Ischemia Reperfusion Injury Mechanism of Dried Ginger-Aconite Decoction Based on Network Pharmacology.Frontiers in pharmacology · 2021Article
- Mindin serves as a tumour suppressor gene during colon cancer progression through MAPK/ERK signalling pathway in mice.Journal of cellular and molecular medicine · 2020Article
- Mindin deficiency alleviates renal fibrosis through inhibiting NF-κB and TGF-β/Smad pathways.Journal of cellular and molecular medicine · 2020Article
Corrections and comments
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Authors and funding
17 authors at 10 institutions in 3 countries.
Funding
Abstract
aimsMindin is a secreted extracellular matrix protein, an integrin ligand, and an angiogenesis inhibitor, other examples of which are all key players in the progression of cardiac hypertrophy. However, its function during cardiac hypertrophy remains unclear. This study was aimed to identify the effect of mindin on cardiac hypertrophy and the underlying mechanisms. METHODS AND
resultsA significant down-regulation of mindin expression was observed in human failing hearts. To further investigate the role of mindin in cardiac hypertrophy, we used cultured neonatal rat cardiomyocytes with gain and loss of mindin function and cardiac-specific Mindin-overexpressing transgenic (TG) mice. In cultured cardiomyocytes, mindin negatively regulated angiotensin II (Ang II)-mediated hypertrophic growth, as detected by [(3)H]-Leucine incorporation, cardiac myocyte area, and hypertrophic marker protein levels. Cardiac hypertrophy in vivo was produced by aortic banding (AB) or Ang II infusion in TG mice and their wild-type controls. The extent of cardiac hypertrophy was evaluated by echocardiography as well as by pathological and molecular analyses of heart samples. Mindin overexpression in the heart markedly attenuated cardiac hypertrophy, fibrosis, and left ventricular dysfunction in mice in response to AB or Ang II. Further analysis of the signalling events in vitro and in vivo indicated that these beneficial effects of mindin were associated with the interruption of AKT/glycogen synthase kinase 3β (GSK3β) and transforming growth factor (TGF)-β1-Smad signalling.
conclusionThe present study demonstrates for the first time that mindin serves as a novel mediator that protects against cardiac hypertrophy and the transition to heart failure by blocking AKT/GSK3β and TGF-β1-Smad signalling.
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