title: Sequential changes in autophagy in diabetic cardiac fibrosis.
abstract: Autophagy is considered to be associated with cardiac fibrosis. However, whether autophagy accelerates or ameliorates fibrosis remains to be elucidated. In the present study, 36 rats were divided into two groups: Control rats and diabetic rats. The diabetic rats were established by feeding the animals a high fat diet combined with streptozotocin. From the two groups, six rats were sacrificed after 1, 6 and 7 months. Cardiac systolic functions were measured. The collagen volume fraction was calculated using Masson's trichome staining and the mRNA expression levels of type‑I and type‑III collagen were measured using reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) to assess the levels of cardiac fibrosis. The protein contents of microtubule‑associated protein 1 light chain 3 (LC3) and sequestosome 1 (P62) were evaluated using western blotting, and the mRNA expression of Beclin 1 was measured using RT‑qPCR, in order to assess autophagy. The results revealed that, in the diabetic rats, cardiac fibrosis developed and cardiac systolic function was reduced. In the hearts of the diabetic rats, the mRNA expression levels of collagen type I and III, and Beclin1 were upregulated; the ratio of the protein level of LC3‑II/LC3‑I was increased and the content of P62 was decreased. All the changes were aggravated as time increased. The changes in autophagy were correlated with those of cardiac fibrosis, suggesting that autophagy may have a synergistic role in diabetic cardiac fibrosis.
authors.affiliation: Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Huikuan
authors.initials: H
authors.lastname: Gao
authors.affiliation: Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Qiong
authors.initials: Q
authors.lastname: Yang
authors.affiliation: Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Ruiqing
authors.initials: R
authors.lastname: Dong
authors.affiliation: Department of Infection, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Fei
authors.initials: F
authors.lastname: Hou
authors.affiliation: Department of Cardiology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, P.R. China.
authors.forename: Yongquan
authors.initials: Y
authors.lastname: Wu
mesh_terms: D000818:Animals; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism; D001343:Autophagy; D000071186:Beclin-1; D015153:Blotting, Western; D003094:Collagen / Q000378:metabolism; D024042:Collagen Type I / Q000378:metabolism; D024061:Collagen Type III / Q000378:metabolism; D003921:Diabetes Mellitus, Experimental / Q000235:genetics / Q000473:pathology* / Q000503:physiopathology; D005355:Fibrosis; D006352:Heart Ventricles / Q000473:pathology / Q000503:physiopathology; D008297:Male; D009206:Myocardium / Q000378:metabolism / Q000473:pathology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation / Q000235:genetics
chemical_list: D051017:Apoptosis Regulatory Proteins; D000071186:Beclin-1; C512829:Becn1 protein, rat; D024042:Collagen Type I; D024061:Collagen Type III; D012333:RNA, Messenger; D003094:Collagen