Cited by 25SARS-CoV-2 and COVID-19 ResearchCOVID-19 Clinical Research StudiesLong-Term Effects of COVID-19

SARS‐CoV‐2 infection aggravates chronic comorbidities of cardiovascular diseases and diabetes in mice

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Ma, Yuanwu, Lu, Dan, Bao, Linlin, Qu, Yajin, Liu, Jiangning, Qi, Xiaolong, Yu, Lei, Zhang, Xu +18 more·2021·Animal Models and Experimental Medicine

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.

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  • COVID-19-related VIS may aggravate age-related pathologies via enhanced SASP-mediated inflammation, as demonstrated for cardiovascular diseases and diabetes in preclinical models, and might further deteriorate immune competence by inducing senescence in immune cells.

    “COVID-19-related VIS may also aggravate age-related pathologies via enhanced SASP-mediated inflammation29,169, as demonstrated for cardiovascular diseases and diabetes in preclinical models170, and might further deteriorate immune competence by inducing senescence in immune cells171,172.”

    From COVID-19 and cellular senescence (2023) · cites this paper as [170]

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  1. [22]Lu D, Ma Y, Zhang W, et al. Knockdown of cytochrome P450 2E1 inhibits oxidative stress and apoptosis in the cTnT(R141W) dilated cardiomyopathy transgenic mice. Hypertension. 2012a; 60: 81‐ 89. 22665122
  2. [23]Lu D, Zhang L, Bao D, et al. Calponin1 inhibits dilated cardiomyopathy development in mice through the epsilonPKC pathway. Int J Cardiol. 2014a; 173: 146‐ 153. 24631115

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Authors
Ma, Y., Lu, D., Bao, L., Qu, Y., Liu, J., Qi, X., Yu, L., Zhang, X., Qi, F., Lv, Q., Liu, Y., Shi, X., Sun, C., Li, J., Wang, J., Han, Y., Gao, K., Dong, W., Liu, N., Gao, S., Xue, J., Wei, Q., Pan, S., Gao, H., Zhang, L., & Qin, C.
Affiliations
  • Chinese Academy of Medical Sciences & Peking Union Medical College (CN)
  • Key Laboratory of Human Disease Comparative Medicine National Health Commission of China (NHC) Institute of Laboratory Animal Science Peking Union Medicine College Chinese Academy of Medical Sciences Beijing China
Corresponding author
Qin, Chuan
Venue
Animal Models and Experimental Medicine
Publisher
Wiley
Published
2021-03
Volume
4
Issue
1
Pages
2-15
ISSN
  • 2096-5451 (ISSN-L)
  • 2576-2095
OpenAlex
W3133881771
Cited by
25
References
35
Citations by year
2026: 1 · 2025: 2 · 2024: 3 · 2023: 8 · 2022: 9 · 2021: 2
FWCI
1.74
Type
journal article
Language
en
Open access
Locations
  • Animal Models and Experimental Medicine (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
Beijing Municipal Natural Science Foundation (M21004)
Topics
  • Health Sciences › Medicine › Infectious Diseases › SARS-CoV-2 and COVID-19 Research
  • Health Sciences › Medicine › Infectious Diseases › COVID-19 Clinical Research Studies
  • Health Sciences › Medicine › Neurology › Long-Term Effects of COVID-19
Keywords
SARS-CoV-2, COVID-19 pandemic, cardiovascular disease, diabetes mellitus, comorbidities, myocardial injury, oxidative stress, apoptosis, insulin resistance, bone mineral density, PI3K/AKT/mTOR pathway, lung infection model
MeSH terms
COVID-19, SARS-CoV-2, Animals, Cardiovascular Diseases, Diabetes Mellitus, Disease Models, Animal, Male, Comorbidity, Diabetes Complications, Mice

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