Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 3 de 3
Filter
1.
EuropePMC; 2020.
Preprint in English | EuropePMC | ID: ppcovidwho-317048

ABSTRACT

SARS-CoV-2 has challenged global healthcare systems in part because its clinical manifestations are heterogeneous. Variable symptoms of SARS-CoV-2 could be attributed to the virus’ ability to mildly induce an innate immune response, as prior transcriptomic data has suggested. Mitochondrial dynamics might partially mediate the effect of SARS-CoV-2 on innate immunity. Many proteins encoded by SARS-CoV have been shown to localize to mitochondria and inhibit Mitochondrial Antiviral Signaling protein (MAVS). We analyzed multiple publicly available RNASeq data in order to unravel the metabolic and mitochondrial transcriptome signature of SARS-CoV-2 in primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report here that SARS-CoV-2 does not dramatically regulate (1) mitochondrial-gene expression or (2) MAVS expression, but (3) downregulates nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex 1 assembly. We also report cell-specific and tissue-specific effects of SARS-CoV-2 on the mitochondrial-encoded and NEM transcriptome that could inform future experimental paradigm selection.

2.
Ann N Y Acad Sci ; 1507(1): 70-83, 2022 01.
Article in English | MEDLINE | ID: covidwho-1673249

ABSTRACT

For many years, it was believed that the aging process was inevitable and that age-related diseases could not be prevented or reversed. The geroscience hypothesis, however, posits that aging is, in fact, malleable and, by targeting the hallmarks of biological aging, it is indeed possible to alleviate age-related diseases and dysfunction and extend longevity. This field of geroscience thus aims to prevent the development of multiple disorders with age, thereby extending healthspan, with the reduction of morbidity toward the end of life. Experts in the field have made remarkable advancements in understanding the mechanisms underlying biological aging and identified ways to target aging pathways using both novel agents and repurposed therapies. While geroscience researchers currently face significant barriers in bringing therapies through clinical development, proof-of-concept studies, as well as early-stage clinical trials, are underway to assess the feasibility of drug evaluation and lay a regulatory foundation for future FDA approvals in the future.


Subject(s)
Aging/genetics , Aging/metabolism , Congresses as Topic/trends , Longevity/physiology , Research Report , Autophagy/physiology , COVID-19/genetics , COVID-19/metabolism , COVID-19/mortality , Cardiovascular Diseases/genetics , Cardiovascular Diseases/metabolism , Cardiovascular Diseases/therapy , Humans , Metabolomics/methods , Metabolomics/trends , Nervous System Diseases/genetics , Nervous System Diseases/metabolism , Nervous System Diseases/therapy , Stem Cell Transplantation/methods , Stem Cell Transplantation/trends
3.
Sci Rep ; 11(1): 3, 2021 01 08.
Article in English | MEDLINE | ID: covidwho-1387457

ABSTRACT

SARS-CoV-2 induces a muted innate immune response compared to other respiratory viruses. Mitochondrial dynamics might partially mediate this effect of SARS-CoV-2 on innate immunity. Polypeptides encoded by open reading frames of SARS-CoV and SARS-CoV-2 have been shown to localize to mitochondria and disrupt Mitochondrial Antiviral Signaling (MAVS) protein signaling. Therefore, we hypothesized that SARS-CoV-2 would distinctly regulate the mitochondrial transcriptome. We analyzed multiple publicly available RNASeq data derived from primary cells, cell lines, and clinical samples (i.e., BALF and lung). We report that SARS-CoV-2 did not dramatically regulate (1) mtDNA-encoded gene expression or (2) MAVS expression, and (3) SARS-CoV-2 downregulated nuclear-encoded mitochondrial (NEM) genes related to cellular respiration and Complex I.


Subject(s)
COVID-19/virology , DNA, Mitochondrial/genetics , Mitochondria/genetics , SARS-CoV-2 , Transcriptome , Cell Line , Humans , Mitochondria/virology
SELECTION OF CITATIONS
SEARCH DETAIL