Disruption of mindin exacerbates cardiac hypertrophy and fibrosis

Zhou Yan Bian, Xiang Wei, Shan Deng, Qi Zhu Tang, Jinghua Feng, Yan Zhang, Chen Liu, Ding Sheng Jiang, Ling Yan, Lian Feng Zhang, Manyin Chen, John Fassett, Yingjie Chen, You Wen He, Qinglin Yang, Peter P. Liu, Hongliang Li

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


Cardiac hypertrophy is a response of the myocardium to increased workload and is characterised by an increase of myocardial mass and an accumulation of extracellular matrix (ECM). As an ECM protein, an integrin ligand, and an angiogenesis inhibitor, all of which are key players in cardiac hypertrophy, mindin is an attractive target for therapeutic intervention to treat or prevent cardiac hypertrophy and heart failure. In this study, we investigated the role of mindin in cardiac hypertrophy using littermate Mindin knockout (Mindin-/-) and wild-type (WT) mice. Cardiac hypertrophy was induced by aortic banding (AB) or angiotensin II (Ang II) infusion in Mindin-/- and WT echocardiography and by pathological and molecular analyses of heart samples. Mindin-/- mice were more susceptible to cardiac hypertrophy and fibrosis in response to AB or Ang II stimulation than wild type. Cardiac function was also markedly exacerbated during both systole and diastole in Mindin-/- mice in response to hypertrophic stimuli.Western blot assays further showed that the activation of AKT/glycogen synthase kinase 3β (GSK3β) signalling in response to hypertrophic stimuli was significantly increased in Mindin-/- mice. Moreover, blocking AKT/GSK3β signalling with a pharmacological AKT inhibitor reversed cardiac abnormalities in Mindin-/- mice. Our data show that mindin, as an intrinsic cardioprotective factor, prevents maladaptive remodelling and the transition to heart failure by blocking AKT/GSK3β signalling.

Original languageEnglish (US)
Pages (from-to)895-910
Number of pages16
JournalJournal of Molecular Medicine
Issue number8
StatePublished - Aug 2012

Bibliographical note

Funding Information:
supported by the National Natural Science Foundation of China (grants

Funding Information:
30900524, 30972954, 81000036 and 81000095) the Support Program for Disciplinary Leaders in Wuhan (200951830561), the Fundamental Research Funds for the Central Universities (3081013) and the National Basic Research Program of China (grant 2011CB503902).


  • AKT
  • Hypertrophy. Remodelling
  • Mindin
  • Signal transduction


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