Protein Arginine Methyltransferases in Cardiovascular and Neuronal Function

Research output: Contribution to journalReview article


External Institution(s)

  • LSU Health Sciences Center - Shreveport
  • University of British Columbia


Original languageEnglish (US)
Pages (from-to)1716-1732
Number of pages17
JournalMolecular Neurobiology
Issue number3
StatusPublished - Mar 1 2020


The methylation of arginine residues by protein arginine methyltransferases (PRMTs) is a type of post-translational modification which is important for numerous cellular processes, including mRNA splicing, DNA repair, signal transduction, protein interaction, and transport. PRMTs have been extensively associated with various pathologies, including cancer, inflammation, and immunity response. However, the role of PRMTs has not been well described in vascular and neurological function. Aberrant expression of PRMTs can alter its metabolic products, asymmetric dimethylarginine (ADMA), and symmetric dimethylarginine (SDMA). Increased ADMA levels are recognized as an independent risk factor for cardiovascular disease and mortality. Recent studies have provided considerable advances in the development of small-molecule inhibitors of PRMTs to study their function under normal and pathological states. In this review, we aim to elucidate the particular roles of PRMTs in vascular and neuronal function as a potential target for cardiovascular and neurological diseases.

    Research areas

  • ADMA, Arginine methylation, Cardiovascular disease, Neurological disease, Protein arginine methyltransferases, Therapeutic target

Citation formats


Couto e Silva, A., Wu, C. Y. C., Citadin, C. T., Clemons, G. A., Possoit, H. L. E., Grames, M. S., ... Lin, H. W. (2020). Protein Arginine Methyltransferases in Cardiovascular and Neuronal Function. Molecular Neurobiology, 57(3), 1716-1732.


Couto e Silva, A, Wu, CYC, Citadin, CT, Clemons, GA, Possoit, HLE, Grames, MS, Lien, CF, Minagar, A, Lee, RHC, Frankel, A & Lin, HW 2020, 'Protein Arginine Methyltransferases in Cardiovascular and Neuronal Function', Molecular Neurobiology, vol. 57, no. 3, pp. 1716-1732.