Mini review ATF4 and GRP78 as novel molecular targets in ER-Stress modulation for critical COVID-19 patients

© 2021. The Author(s), under exclusive licence to Springer Nature B.V..

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and has resulted in more than 4.4 million deaths worldwide as of August 24, 2021. Viral infections such as SARS-CoV2 are associated with endoplasmic reticulum (ER) stress and also increased the level of reactive oxygen species. Activating transcription factor 4 (ATF4) is preferentially translated under integrated stress conditions and controls the genes involved in protein homeostasis, amino acid transport and metabolism, and also protection from oxidative stress. The GRP78, regulated either directly or indirectly by ATF4, is an essential chaperone in the ER and overexpressed and appears on the surface of almost all cells during stress and function as a SARS-CoV2 receptor. In this mini-review article, we briefly discuss the effects of SARS-CoV2 infection on the ER stress, and then the stress modulator functions of ATF4 and GRP78 as novel therapeutic targets were highlighted. Finally, the effects of GRP78 inhibitory components as potential factors for targeted therapies for COVID-19 critical cases were discussed.

Medienart:

E-Artikel

Erscheinungsjahr:

2022

Erschienen:

2022

Enthalten in:

Zur Gesamtaufnahme - volume:49

Enthalten in:

Molecular biology reports - 49(2022), 2 vom: 13. Feb., Seite 1545-1549

Sprache:

Englisch

Beteiligte Personen:

Shahriari-Felordi, Mahtab [VerfasserIn]
Alikhani, Hani Keshavarz [VerfasserIn]
Hashemian, Seyed-Mohammad Reza [VerfasserIn]
Hassan, Moustapha [VerfasserIn]
Vosough, Massoud [VerfasserIn]

Links:

Volltext

Themen:

145891-90-3
ATF4
ATF4 protein, human
Activating Transcription Factor 4
COVID-19 disease
ER stress modulation
Endoplasmic Reticulum Chaperone BiP
GRP78 targeting
HSPA5 protein, human
Journal Article
Review

Anmerkungen:

Date Completed 17.02.2022

Date Revised 17.02.2022

published: Print-Electronic

Citation Status MEDLINE

doi:

10.1007/s11033-021-07071-9

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM335637116