SARS‐CoV‐2 infection aggravates chronic comorbidities of cardiovascular diseases and diabetes in mice. Issue 1 (6th March 2021)

• Record Type: Journal Article
• Authors: Ma, Yuanwu; Lu, Dan; Bao, Linlin; Qu, Yajin; Liu, Jiangning; Qi, Xiaolong; Yu, Lei; Zhang, Xu; Qi, Feifei; Lv, Qi; Liu, Yunpeng; Shi, Xudong; Sun, Caixian; Li, Jing; Wang, Jie; Han, Yunlin; Gao, Kai; Dong, Wei; Liu, Ning; Gao, Shan; Xue, Jing; Wei, Qiang; Pan, Sidan; Gao, Hong; Zhang, Lianfeng; Qin, Chuan
• Is Part Of: Animal models and experimental medicine. Volume 4:Issue 1(2021)
• Page Start: 2
• Page End: 15
• Publication Date: 2021-03-06
• Subjects: Cardiovascular disease -- COVID‐19 -- diabetes mellitus -- mouse model -- SARS‐CoV‐2; Laboratory animals -- Periodicals; Diseases -- Animal models -- Periodicals; Animal models in research -- Periodicals; Veterinary medicine -- Periodicals; Laboratory Animal Science; Disease Models, Animal; Animals, Laboratory; Animal Welfare; Veterinary Medicine; Animal models in research; Diseases -- Animal models; Laboratory animals; Veterinary medicine; Periodicals; Fulltext; Internet Resources; Periodicals; Periodicals; 616.0273
• DOI: 10.1002/ame2.12155
• Languages: English
• ISSNs: 2576-2095

Abstract

Abstract: Background: Cardiovascular diseases (CVDs) and diabetes mellitus (DM) are top two chronic comorbidities that increase the severity and mortality of COVID‐19. However, how SARS‐CoV‐2 alters the progression of chronic diseases remain unclear. Methods: We used adenovirus to deliver h‐ACE2 to lung to enable SARS‐CoV‐2 infection in mice. SARS‐CoV‐2's impacts on pathogenesis of chronic diseases were studied through histopathological, virologic and molecular biology analysis. Results: Pre‐existing CVDs resulted in viral invasion, ROS elevation and activation of apoptosis pathways contribute myocardial injury during SARS‐CoV‐2 infection. Viral infection increased fasting blood glucose and reduced insulin response in DM model. Bone mineral density decreased shortly after infection, which associated with impaired PI3K/AKT/mTOR signaling. Conclusion: We established mouse models mimicked the complex pathological symptoms of COVID‐19 patients with chronic diseases. Pre‐existing diseases could impair the inflammatory responses to SARS‐CoV‐2 infection, which further aggravated the pre‐existing diseases. This work provided valuable information to better understand the interplay between the primary diseases and SARS‐CoV‐2 infection.