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• W4378649852 abstract "Background: As the pandemic persists, post-acute sequelae of CoV-2 (PACS) including cardiovascular manifestations have emerged as a new health threat. Obesity is an established risk factor for acute COVID-19 severity. Evolving evidence has suggested its contributive roles in the pathogenesis of PACS. However, whether and how obesity can exacerbate PACS-related cardiomyopathy is unknown. Methods: A Spike protein-pseudotyped (Spp) virus with the proper surface tropism of SARS-CoV- 2 was developed for viral entry assay in vitro and administration into high fat diet (HFD)-fed mice. The systemic viral loads and cardiac transcriptomes were analyzed at 2 and 24 hrs, 3, 6, and 24 weeks post infection (wpi) using RNA-seq or real time RT-PCR. Echocardiography was used to monitor cardiac functions. Results: Low-density lipoprotein cholesterol enhanced viral uptake in endothelial cells, macrophages, and cardiomyocyte-like H9C2 cells. Selective cardiac and adipose viral depositions were observed in HFD mice but not in normal-chow-fed mice. The cardiac transcriptional signatures in HFD mice at 3, 6, and 24 wpi showed systemic suppression of mitochondria respiratory gene families including ATP synthases and nicotinamide adenine dinucleotide:ubiquinone oxidoreductase gene members, upregulation of stress pathway-related crucial factors such as nuclear factor-erythroid 2-related factor 1, and increases in expression of glucose metabolism-associated genes. Cardiac ejection fraction and fractional shortening were significantly decreased, while left ventricular end-systolic diameter and volume were significantly increased, in HFD mice at 24 wpi as compared with the age-matched HFD control mice. Conclusion: Our data demonstrated that chronic cardiac inflammations were persisted and exaggerated in HFD mice after viral infection, leading to mitochondrial metabolic perturbations and myocardial contractile impairment. This work was supported by grants from the National Institutes of Health (AR073172 and NIH COBRE (P20GM109091) pilot study to W.T., NSF EPSCoR (OIA1736150) to H.K., HL160541 to T.C.). This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process." @default.
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• W4378649852 date "2023-05-01" @default.
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• W4378649852 title "The Spike protein of SARS-CoV-2 exacerbates cardiac mitochondrial dysfunctions in obese mice: mechanistic evidence for cardiomyopathy in post-acute sequelae of COVID-19" @default.
• W4378649852 doi "https://doi.org/10.1152/physiol.2023.38.s1.5688802" @default.
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