The inflammasome promotes adverse cardiac remodeling following acute myocardial infarction in the mouse

By E. Mezzaroma, S. Toldo, D. Farkas, I. Seropian, B. V. Van Tassell, Fadi N. Salloum, Harsha R. Kannan, Angela C Menna, N. Voelkel, Antonio Abbate. Proceedings of the National Academy of Sciences of the United States of America, 2011

602 citations recorded by the source corpus.

Subfields: Cardiology and Cardiovascular Medicine, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/c15ad409b7bb31ba7b93ea6b41e4e59ffd8c846c

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cardiology and Cardiovascular Medicine

1. Nikolaos G. Frangogiannis
2. Sumanth D. Prabhu
3. D. Hausenloy
4. M. Krenz
5. Ronald J. Korthuis
6. Christopher P. Baines
7. Theodore J Kalogeris

In Molecular Biology

1. Nikolaos G. Frangogiannis
2. Sumanth D. Prabhu
3. S. Toldo
4. Antonio Abbate
5. D. Hausenloy

In Surgery

1. Nikolaos G. Frangogiannis
2. Sumanth D. Prabhu

Citations in the corpus

• Inflammation following acute myocardial infarction: Multiple players, dynamic roles, and novel therapeutic opportunities (2018, background): “NLRP3 inflammasomes Experimental rodent studies have shown that genetic and pharmacological inhibition of the NLRP3 inflammasome may reduce MI size and prevent adverse LV remodeling (Coll et al., 2015; Kawaguchi et al., 2011; Marchetti et al., 2014; Mezzaroma et al., 2011; Pomerantz et al., 2001; Sa”
• Pathophysiology of Myocardial Infarction (2015, positive): “pyrin domain 3 (NLRP3) inflammasome in the infarcted myocardium (191, 253), localized in leukocytes, fibroblasts, and border zone cardiomyocytes (191, 253, 315).”
• The NLRP3 inflammasome in acute myocardial infarction (2018, background): “AIR-HF (2012) Stable NYHA class II–III systolic HF with CRP >2 mg/l (10) Single-arm, open-label treatment with anakinra (100 mg once daily for 2 weeks) • Reduction in CRP levels • Improvement in peak aerobic exercise capacity at 2 weeks • Improvement in ventilator efficiency at 2 weeks 73”
• The Biological Basis for Cardiac Repair After Myocardial Infarction: From Inflammation to Fibrosis. (2016, background): “remodeling and dysfunction in vivo after nonreperfused MI in mice.(87) Hence, the NLRP3 inflammasome is a key mediator of”