Preservation of Contractile Reserve and Diastolic Function by Inhibiting the NLRP3 Inflammasome with OLT1177® (Dapansutrile) in a Mouse Model of Severe …

J Aliaga, A Bonaventura, E Mezzaroma, Y Dhakal… - Molecules, 2021 - mdpi.com
Interleukin-1β (IL-1β), a product of the NLRP3 inflammasome, modulates cardiac contractility
and diastolic function. We proposed that OLT1177®(dapansutrile), a novel NLRP3 inhibitor …

The NLRP3 inflammasome inhibitor, OLT1177 (dapansutrile), reduces infarct size and preserves contractile function after ischemia reperfusion injury in the mouse

S Toldo, AG Mauro, Z Cutter… - Journal of …, 2019 - journals.lww.com
Background: Activation of the NLRP3 inflammasome is a primary driver of sterile
inflammation in response to myocardial ischemia reperfusion. Pharmacologic inhibitors of …

Pharmacologic inhibition of the NLRP3 inflammasome preserves cardiac function after ischemic and nonischemic injury in the mouse

C Marchetti, S Toldo, J Chojnacki… - Journal of …, 2015 - journals.lww.com
Background: Sterile inflammation resulting from myocardial injury activates the NLRP3
inflammasome and amplifies the inflammatory response mediating further damage …

The selective NLRP3-inflammasome inhibitor MCC950 reduces infarct size and preserves cardiac function in a pig model of myocardial infarction

GPJ Van Hout, L Bosch, GHJM Ellenbroek… - European heart …, 2017 - academic.oup.com
Aims Myocardial infarction (MI) triggers an intense inflammatory response that is associated
with infarct expansion and is detrimental for cardiac function. Interleukin (IL)-1β and IL-18 …

The selective NLRP3-inflammasome inhibitor MCC950 reduces myocardial fibrosis and improves cardiac remodeling in a mouse model of myocardial infarction

R Gao, H Shi, S Chang, Y Gao, X Li, C Lv… - International …, 2019 - Elsevier
Abstract Background/Aims. Early inflammatory responses after myocardial infarction (MI) are
likely to increase myocardial fibrosis and subsequent cardiac remodeling. MCC950, a …

NLRP3-Inflammasome Inhibition with IZD334 Does Not Reduce Cardiac Damage in a Pig Model of Myocardial Infarction

MJM Silvis, EJ Demkes, L Timmers, F Arslan… - Biomedicines, 2022 - mdpi.com
NLRP3-inflammasome-mediated signaling is thought to significantly contribute to the extent
of myocardial damage after myocardial infarction (MI). The purpose of this study was to …

Inhibition of the NLRP3 inflammasome limits the inflammatory injury following myocardial ischemia–reperfusion in the mouse

S Toldo, C Marchetti, AG Mauro, J Chojnacki… - International Journal of …, 2016 - Elsevier
Background Successful reperfusion is the most effective strategy to reduce ischemic injury in
acute myocardial infarction (AMI). Ischemic injury, however, also triggers a secondary …

Role of NLRP3 inflammasome in cardiac inflammation and remodeling after myocardial infarction

M Takahashi - Biological and Pharmaceutical Bulletin, 2019 - jstage.jst.go.jp
An accumulating body of evidence indicates that inflammation plays a crucial role in the
pathophysiology of myocardial infarction (MI). Nucleotide-binding oligomerization domain …

Inhibiting NLRP3 inflammasome activity in acute myocardial infarction: a review of pharmacologic agents and clinical outcomes

LF Buckley, P Libby - Journal of Cardiovascular Pharmacology, 2019 - journals.lww.com
The NLRP3 inflammasome is an intracellular, multimeric protein complex that initiates a
potent inflammatory response to danger signals. After acute myocardial infarction, NLRP3 …

The Nlrp3 inflammasome promotes myocardial dysfunction in structural cardiomyopathy through interleukin‐1β

NA Bracey, PL Beck, DA Muruve… - Experimental …, 2013 - Wiley Online Library
New findings• What is the central question of this study? Heart failure is associated with
persistent sterile inflammation that worsens disease severity; however, the molecular …