Four AGTR2 gene variants (rs200599388, rs1556673810, rs3729979, rs1556673736) were identified as highly deleterious, causing structural instability linked to cardiovascular diseases.
In silico analysis identified four specific nsSNPs in the AGTR2 gene that cause structural instability, highlighting potential therapeutic targets for cardiovascular diseases.
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Background and Aim Nonsynonymous single nucleotide polymorphisms (nsSNPs) in angiotensin Type II receptor ( AGTR2 ) have been identified as a potential cause of cardiovascular illness in humans. Identifying structurally and functionally relevant alterations in AGTR2 is critical to investigate possible therapeutic targets. Methods A comprehensive computational pipeline was employed to evaluate deleterious nsSNPs using multiple prediction algorithms, including SIFT, PolyPhen‐2, CADD, REVEL, Mutation Assessor, MetaLR, I‐Mutant, MutPred, and Phylo3D. Molecular docking and molecular dynamic simulation strategies were further utilized to thoroughly validate these nsSNPs. Additionally, gene–gene interaction networks were constructed to explore AGTR2 ′s functional associations. Results Our findings indicated that four nsSNPs, including rs200599388, rs1556673810, rs3729979, and rs1556673736, potentially have the most deleterious effect on the AGTR2 gene. MD simulations revealed that these variants induced increased structural fluctuations and conformational instability compared with the wild‐type protein. Gene–gene interaction analysis indicated that AGTR2 participates in several key regulatory pathways relevant to cardiovascular physiology. Conclusion These findings will form the basis to design precision medicines for cardiovascular diseases in the future and welcome further preclinical and clinical investigations.
Iqbal et al. (Thu,) reported a other. Four AGTR2 gene variants (rs200599388, rs1556673810, rs3729979, rs1556673736) were identified as highly deleterious, causing structural instability linked to cardiovascular diseases.