Depletion of Kindlin-2 induces cardiac dysfunction in mice.

Sci China Life Sci 2016 Nov 20;59(11):1123-1130. Epub 2016 Sep 20.

Department of Human Anatomy, Histology and Embryology, and Key Laboratory of Carcinogenesis and Translational Research, Ministry of Education, Peking University Health Science, and State Key Laboratory of Natural and Biomimetic Drugs, Peking University Health Science Center, Beijing, 100191, China.

Kindlin-2, a member of the Kindlin family focal adhesion proteins, plays an important role in cardiac development. It is known that defects in the Z-disc proteins lead to hypertrophic cardiomyopathy (HCM) or dilated cardiomyopathy (DCM). Our previous investigation showed that Kindlin-2 is mainly localized at the Z-disc and depletion of Kindlin-2 disrupts the structure of the Z-Disc. Here, we reported that depletion of Kindlin-2 leads to the disordered myocardial fibers, fractured and vacuolar degeneration in myocardial fibers. Interestingly, depletion of Kindlin-2 in mice induced cardiac myocyte hypertrophy and increased the heart weight. Furthermore, decreased expression of Kindlin-2 led to cardiac dysfunction and also markedly impairs systolic function. Our data indicated that Kindlin-2 not only maintains the cardiac structure but also is required for cardiac function.

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http://dx.doi.org/10.1007/s11427-016-0025-0DOI Listing
November 2016
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