Gastrointestinal, Liver, Pancreas, Oral and Psychological Long-term Symptoms of COVID-19 After Recovery: A Review.

Autor:	Afrisham R; Department of Clinical Laboratory Sciences, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran., Jadidi Y; Department of Clinical Laboratory Sciences, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran., Davoudi M; Department of Clinical Laboratory Sciences, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran., Moayedi K; Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran., Soliemanifar O; Department of Education in the City of Khorramshahr, General Department of Education in Khuzestan Province, Iran., Eleni Xirouchaki C; Monash Biomedicine Discovery Institute, Monash University, Clayton, Victoria-3800, Australia.; Department of Biochemistry and Molecular Biology, Monash University, Clayton, Victoria-3800, Australia., Ashtary-Larky D; Nutrition and Metabolic Diseases Research Center, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran., Seyyedebrahimi S; Department of Clinical Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran., Alizadeh S; Department of Hematology, School of Allied Medicine, Tehran University of Medical Sciences, Tehran, Iran.
Jazyk:	angličtina
Zdroj:	Mini reviews in medicinal chemistry [Mini Rev Med Chem] 2023; Vol. 23 (7), pp. 852-868.
DOI:	10.2174/1389557523666221116154907
Abstrakt:	Due to the importance of control and prevention of COVID-19-correlated long-term symptoms, the present review article has summarized what has been currently known regarding the molecular and cellular mechanisms linking COVID-19 to important long-term complications including psychological complications, liver and gastrointestinal manifestations, oral signs as well as even diabetes. COVID-19 can directly affect the body cells through their Angiotensin-converting enzyme 2 (ACE-2) to induce inflammatory responses and cytokine storm. The cytokines cause the release of reactive oxygen species (ROS) and subsequently initiate and promote cell injuries. Another way, COVID-19-associated dysbiosis may be involved in GI pathogenesis. In addition, SARS-CoV-2 reduces butyrate-secreting bacteria and leads to the induction of hyperinflammation. Moreover, SARS-CoV-2-mediated endoplasmic reticulum stress induces de novo lipogenesis in hepatocytes, which leads to hepatic steatosis and inhibits autophagy via increasing mTOR. In pancreas tissue, the virus damages beta-cells and impairs insulin secretion. SARS-COV-2 may change the ACE2 activity by modifying ANGII levels in taste buds which leads to gustatory dysfunction. SARS-CoV-2 infection and its resulting stress can lead to severe inflammation that can subsequently alter neurotransmitter signals. This, in turn, negatively affects the structure of neurons and leads to mood and anxiety disorders. In conclusion, all the pathways mentioned earlier can play a crucial role in the disease's pathogenesis and related comorbidities. However, more studies are needed to clarify the underlying mechanism of the pathogenesis of the new coming virus. (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)
Databáze:	MEDLINE
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