Back to Search
Start Over
Molecular Mechanism of Acute Sarcopenia in Elderly Patient with COVID - 19
- Source :
- Acta Medica Indonesiana, Vol 53, Iss 4 (2022)
- Publication Year :
- 2022
- Publisher :
- Interna Publishing, 2022.
-
Abstract
- Coronavirus Disease 2019 (COVID-19) is an infectious disease caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). Case fatality rate has been on the rise among older adults. Muscle loss is a consequence of several chronic diseases (chronic sarcopenia) and recent theory also suggested that acute sarcopenia may caused by acute significant stressor such as an acute illness, surgery, infections, trauma or burns including COVID-19 infection leading to further muscle loss in elderly. Cytokine storm, the hallmark of COVID-19 pathogenesis will induce various pro-inflammatory cytokine such as IL-1 and IL-6 causing acute sarcopenia by activating negative regulators like NF-κB, atrogin-1, MURF-1. Long standing chronic inflammation also known as inflammaging along with acute inflammation during COVID-19 in elderly will cause reticulum endoplasmic and mitochondria stress activating caspase and finally increase both cytosolic and nuclear levels of AIF and EndoG to induce acute sarcopenia. Several precipitating factors shared same molecular pathway like physical inactivity and hormonal dysregulation which act through IGF-1-AKT-mTOR pathway. Physical inactivity during COVID-19 infection also induced myostatin and Atrogin-1/ MaFbx/ MuRF pathway. This review provides recent research advances dealing with molecular pathway modulating muscle mass in acute sarcopenia during COVID-19 infection.
- Subjects :
- covid-19
acute sarcopenia
inflammation
aging
Internal medicine
RC31-1245
Subjects
Details
- Language :
- English
- ISSN :
- 01259326 and 23382732
- Volume :
- 53
- Issue :
- 4
- Database :
- Directory of Open Access Journals
- Journal :
- Acta Medica Indonesiana
- Publication Type :
- Academic Journal
- Accession number :
- edsdoj.651534d0de542e4bc60c30b3f97268b
- Document Type :
- article