Journal Article Review Epublish 1 citation
PubMed: 39727939 DOI: 10.3390/cimb46120811
Neurological Sequelae of Post-COVID-19 Fatigue: A Narrative Review of Dipeptidyl Peptidase IV-Mediated Cerebrovascular Complications.
Curr Issues Mol Biol 46(12):13565-13582
Authors: Che Mohd Nasril Che Mohd Nassir, Muhammad Danial Che Ramli, Usman Jaffer, Hafizah Abdul Hamid, Muhammad Zulfadli Mehat, Mazira Mohamad Ghazali, Ebrahim Nangarath Kottakal Cheriya
Affiliations
- Department of Anatomy and Physiology, Faculty of Medicine, School of Basic Medical Sciences, Universiti Sultan Zainal Abidin, Kuala Terengganu 20400, Terengganu, Malaysia.
- Faculty of Health and Life Sciences, Management and Science University, Shah Alam 40150, Selangor, Malaysia.
- Kulliyyah of Islamic Revealed Knowledge and Human Sciences, International Islamic University Malaysia, Kuala Lumpur 50728, Malaysia.
- Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia (UPM), Serdang 43400, Selangor, Malaysia.
- Department of Anatomy and Physiology, Faculty of Medicine, School of Basic Medical Sciences, Universiti Sultan Zainal Abidin, Kuala Terengganu 20400, Terengganu, Malaysia. Department of Neurosciences, School of Medical Sciences, Universiti Sains Malaysia, Kubang Kerian, Kota Bharu 16150, Kelantan, Malaysia.
- Department of Physiology, International Medical School (IMS), Management and Science University, Shah Alam 40150, Selangor, Malaysia.
Abstract
Coronavirus disease 2019 (COVID-19) has been a global pandemic affecting millions of people's lives, which has led to 'post-COVID-19 fatigue'. Alarmingly, severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) not only infects the lungs but also influences the heart and brain. Endothelial cell dysfunction and hypercoagulation, which we know occur with this infection, lead to thrombo-inflammation that can manifest as many myriad cardio-cerebrovascular disorders, such as brain fog, fatigue, cognitive dysfunction, etc. Additionally, SARS-CoV-2 has been associated with oxidative stress, protein aggregation, cytokine storm, and mitochondrial dysfunction in neurodegenerative diseases. Accordingly, the identification of molecular targets involved in these actions could provide strategies for preventing and treating this disease. In particular, the very common enzyme dipeptidyl peptidase IV (DPPIV) has recently been identified as a candidate co-receptor for the cell entry of the SARS-CoV-2 virus with its involvement in infection. In addition, DPPIV has been reported as a co-receptor for some viruses such as Middle East respiratory syndrome-coronavirus (MERS-CoV). It mediates immunologic reactions and diseases such as type 2 diabetes mellitus, obesity, and hypertension, which have been considered the prime risk factors for stroke among other types of cardio-cerebrovascular diseases. Unlike angiotensin-converting enzyme 2 (ACE2), DPPIV has been implicated in aggravating the course of infection due to its disruptive effect on inflammatory signaling networks and the neuro-glia-vascular unit. Regarding the neurological, physiological, and molecular grounds governing post-COVID-19 fatigue, this review focuses on DPPIV as one of such reasons that progressively establishes cerebrovascular grievances following SARS-CoV infection.
MeSH
Diabetes Mellitus, Cells, Coronavirus, Sars-Cov-2, Dipeptidyl Peptidase 4, Brain, Covid-19, Enzymes, Fatigue, Viruses, Cerebrovascular Disorders, Peptide Hydrolases, Middle East Respiratory Syndrome Coronavirus, Neurodegenerative Diseases, Infections, Diabetes Mellitus, Type 2