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NLRP3 inflammasome in cardiovascular diseases: Pathophysiological and pharmacological implications.

Abstract
Growing evidence points out the importance of nucleotide-binding oligomerization domain leucine-rich repeat and pyrin domain-containing protein 3 (NLRP3) inflammasome in the pathogenesis of cardiovascular diseases (CVDs), including hypertension, myocardial infarct (MI), ischemia, cardiomyopathies (CMs), heart failure (HF), and atherosclerosis. In this regard, intensive research efforts both in humans and in animal models of CVDs are being focused on the characterization of the pathophysiological role of NLRP3 inflammasome signaling in CVDs. In addition, clinical and preclinical evidence is coming to light that the pharmacological blockade of NLRP3 pathways with drugs, including novel chemical entities as well as drugs currently employed in the clinical practice, biologics and phytochemicals, could represent a suitable therapeutic approach for prevention and management of CVDs. On these bases, the present review article provides a comprehensive overview of clinical and preclinical studies about the role of NLRP3 inflammasome in the pathophysiology of CVDs, including hypertension, MI, ischemic injury, CMs, HF and atherosclerosis. In addition, particular attention has been focused on current evidence on the effects of drugs, biologics, and phytochemicals, targeting different steps of inflammasome signaling, in CVDs.
AuthorsCarolina Pellegrini, Alma Martelli, Luca Antonioli, Matteo Fornai, Corrado Blandizzi, Vincenzo Calderone
JournalMedicinal research reviews (Med Res Rev) Vol. 41 Issue 4 Pg. 1890-1926 (07 2021) ISSN: 1098-1128 [Electronic] United States
PMID33460162 (Publication Type: Journal Article, Review)
Copyright© 2021 Wiley Periodicals LLC.
Chemical References
  • Inflammasomes
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Phytochemicals
Topics
  • Animals
  • Cardiovascular Diseases (drug therapy)
  • Humans
  • Inflammasomes
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Phytochemicals
  • Signal Transduction

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