title: PDCD5 protects against cardiac remodeling by regulating autophagy and apoptosis.
abstract: Cardiac remodeling, including cardiac hypertrophy and fibrosis, is an important pathological process that can lead to heart failure. A previous study demonstrated that autophagy could represent an active adaptive response in cardiomyocytes that affords protection from cardiac remodeling. In the present study, we investigated the role of an autophagy-related gene, PDCD5 (Programmed cell death 5), in cardiac remodeling induced by β-adrenergic stimulation in vivo. We report for the first time that mice systemically overexpressing PDCD5 (PDCD5tg) were protected from cardiac remodeling. In addition, cardiac function was preserved in PDCD5tg mice in response to isoproterenol (ISO) stimulation. Importantly, basal autophagy was significantly higher in PDCD5tg mice than in the wild-type (WT) mice. Moreover, apoptosis was significantly lower in PDCD5tg mice than in WT mice, among the ISO-induced animals. In summary, our findings reveal that PDCD5 overexpression improves cardiac function and inhibits cardiac remodeling induced by ISO via induction of autophagy and inhibition of apoptosis.
authors.affiliation: Department of Cardiology, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education and Beijing Key Laboratory of Cardiovasicular Receptors Research, Beijing 100191, China.
authors.forename: Shu
authors.initials: S
authors.lastname: Zhang
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Ge
authors.initials: G
authors.lastname: Li
authors.affiliation: Department of Cardiology, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education and Beijing Key Laboratory of Cardiovasicular Receptors Research, Beijing 100191, China.
authors.forename: Xin
authors.initials: X
authors.lastname: Fu
authors.affiliation: Department of Cardiology, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education and Beijing Key Laboratory of Cardiovasicular Receptors Research, Beijing 100191, China.
authors.forename: Yanchao
authors.initials: Y
authors.lastname: Qi
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Mengtao
authors.initials: M
authors.lastname: Li
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Guang
authors.initials: G
authors.lastname: Lu
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Hu
authors.affiliation: Department of Cardiology, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education and Beijing Key Laboratory of Cardiovasicular Receptors Research, Beijing 100191, China.
authors.forename: Nan
authors.initials: N
authors.lastname: Wang
authors.affiliation: Key Laboratory of Medical Immunology, Ministry of Health, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Yingyu
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
authors.forename: Yun
authors.initials: Y
authors.lastname: Bai
authors.affiliation: Department of Cardiology, Peking University Third Hospital and Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Ministry of Health, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education and Beijing Key Laboratory of Cardiovasicular Receptors Research, Beijing 100191, China. Electronic address: mingcui@bjmu.edu.cn.
authors.forename: Ming
authors.initials: M
authors.lastname: Cui
mesh_terms: D000818:Animals; D017209:Apoptosis; D051017:Apoptosis Regulatory Proteins / Q000235:genetics*; D001343:Autophagy; D006332:Cardiomegaly / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D005355:Fibrosis / Q000235:genetics / Q000473:pathology; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D009363:Neoplasm Proteins / Q000235:genetics*; D015854:Up-Regulation; D020257:Ventricular Remodeling
chemical_list: D051017:Apoptosis Regulatory Proteins; D009363:Neoplasm Proteins; C486488:Pdcd5 protein, mouse
keywords: Autophagy; Cardiac remodeling; PDCD5