Extracellular nucleotide regulation and signaling in cardiac fibrosis

Tatiana Novitskaya, Elena Chepurko, Roman Covarrubias, Sergey Novitskiy, Sergey V. Ryzhov, Igor Feoktistov, Richard J. Gumina

Research output: Contribution to journalReview articlepeer-review

20 Scopus citations


Following myocardial infarction, purinergic nucleotides and nucleosides are released via non-specific and specific mechanisms in response to cellular activation, stress, or injury. These extracellular nucleotides are potent mediators of physiologic and pathologic responses, contributing to the inflammatory and fibrotic milieu within the injured myocardium. Via autocrine or paracrine signaling, cell-specific effects occur through differentially expressed purinergic receptors of the P2X, P2Y, and P1 families. Nucleotide activation of the ionotropic (ligand-gated) purine receptors (P2X) and several of the metabotropic (G-protein-coupled) purine receptors (P2Y) or adenosine activation of the P1 receptors can have profound effects on inflammatory cell function, fibroblast function, and cardiomyocyte function. Extracellular nucleotidases that hydrolyze released nucleotides regulate the magnitude and duration of purinergic signaling. While there are numerous studies on the role of the purinergic signaling pathway in cardiovascular disease, the extent to which the purinergic signaling pathway modulates cardiac fibrosis is incompletely understood. Here we provide an overview of the current understanding of how the purinergic signaling pathway modulates cardiac fibroblast function and myocardial fibrosis.

Original languageEnglish (US)
Pages (from-to)47-56
Number of pages10
JournalJournal of Molecular and Cellular Cardiology
StatePublished - Apr 1 2016
Externally publishedYes


  • Adenosine
  • Adenosine triphosphate
  • Cardiac fibrosis
  • Ectonucleotidase
  • Purinergic receptors

ASJC Scopus subject areas

  • Molecular Biology
  • Cardiology and Cardiovascular Medicine


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