Apelin as a new therapeutic target for COVID-19

Abstract

Endogenous neuropeptide apelin13 engages in a number of physiological processes in the heart, lungs, and other peripheral organs via binding to the G-protein-coupled receptor apj. Angiotensin converting enzyme 2 (ACE2), which is known to function as a viral receptor that initiates the early phases of SARS-CoV-2 infection, has the ability to bind to apelin13 and be destroyed by it. The purpose of this work was to investigate if apelin, by preventing ACE2 from binding to the SARS-CoV-2 spike protein, has a protective role during the infection phase. We carried out a cell-cell fusion assay with ACE2 expressing cells and S protein expressing cells to see if Apelin13 reduces ACE2 binding to the SARS-CoV-2 spike protein (S protein). Apelin13 therapy prevents cell-cell fusion in this experiment, which is caused by ACE2 binding to S protein. Then we created lentiviruses with false typing that produce S protein. The human bronchial epithelial cell lines were infected with this pseudovirus. Apelin13 shielded these cells from the viral infection in our experiment. The amount of viral spike expression decreased in the presence of Apelin13 in a concentration-dependent way. Additionally, we looked examined publically accessible transcriptome data with an emphasis on Apelin13's advantageous effects on the lung. Apelin13 may regulate inflammatory reactions to viral infection by decreasing the NF-KB (Nuclear Factor-Kappa-B) pathway, according to transcriptome research. In conclusion, Apelin13 is a potential therapeutic candidate for SARS-CoV-2 infection.