title: Depletion of Kindlin-2 induces cardiac dysfunction in mice.
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.
authors.affiliation: 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.
authors.forename: Lihua
authors.initials: L
authors.lastname: Qi
authors.affiliation: 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.
authors.forename: Yu
authors.initials: Y
authors.lastname: Yu
authors.affiliation: 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.
authors.forename: Xiaochun
authors.initials: X
authors.lastname: Chi
authors.affiliation: 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.
authors.forename: Danyu
authors.initials: D
authors.lastname: Lu
authors.affiliation: Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Peking University Health Science, Beijing, 100191, China.
authors.forename: Yao
authors.initials: Y
authors.lastname: Song
authors.affiliation: Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Peking University Health Science, Beijing, 100191, China.
authors.forename: Youyi
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: 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. Hongquan.Zhang@bjmu.edu.cn.
authors.forename: Hongquan
authors.initials: H
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001794:Blood Pressure; D015153:Blotting, Western; D003598:Cytoskeletal Proteins / Q000235:genetics* / Q000378:metabolism; D004452:Echocardiography; D006321:Heart / Q000503:physiopathology*; D008297:Male; D008813:Mice, Inbred ICR; D018613:Microscopy, Confocal; D009124:Muscle Proteins / Q000235:genetics* / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000473:pathology; D009929:Organ Size / Q000235:genetics; D034622:RNA Interference; D013997:Time Factors
chemical_list: D003598:Cytoskeletal Proteins; D009124:Muscle Proteins; C527802:kindlin-2 protein, mouse
keywords: Kindlin-2; cardiac dysfunction; depletion; mouse; myocardial hypertrophy