Depletion of Kindlin-2 induces cardiac dysfunction in mice View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-11

AUTHORS

Lihua Qi, Yu Yu, Xiaochun Chi, Danyu Lu, Yao Song, Youyi Zhang, Hongquan Zhang

ABSTRACT

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. More... »

PAGES

1123-1130

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s11427-016-0025-0

DOI

http://dx.doi.org/10.1007/s11427-016-0025-0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1051865522

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/27722852


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