English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

At global level, the pandemic coronavirus disease 2019 (COVID-19) is known to be caused by an etiologic agent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Numerous evidence and propositions have emerged on the molecular and cellular attributes that cause COVID-19. Notwithstanding, still several key questions with reference to molecular aspects of severity of infection by SARS-CoV-2 need to be answered. In the same line, the role of healthy mitochondria to maintain intracellular temperature and their association with the severity of SARS-CoV-2 is completely missing. In this direction, preclinical and clinical data on the comorbidities in the case of mitochondrial defective disease and COVID-19 are not available. The authors propose that patients harboring primary mitochondrial disease and secondary mitochondrial dysfunction will display a higher severity and death rate compared to healthy mitochondria harboring patients.

Do compromised mitochondria aggravate severity and fatality by SARS-CoV-2?