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JACC Basic Transl Sci. 2017 Aug 28;2(4):418-430. doi: 10.1016/j.jacbts.2017.06.005. eCollection 2017 Aug.

The IL-1β Antibody Gevokizumab Limits Cardiac Remodeling and Coronary Dysfunction in Rats With Heart Failure.

Harouki N1,2,3, Nicol L1,2,3,4, Remy-Jouet I1,2,3, Henry JP1,2,3, Dumesnil A1,2,3, Lejeune A1,2,3, Renet S1,2,3, Golding F1,2,3, Djerada Z1,2,3,5, Wecker D6, Bolduc V7, Bouly M7, Roussel J7, Richard V1,2,3, Mulder P1,2,3,4.

Author information

INSERM U1096, Rouen, France.
Normandy University, IRIB, Rouen, France.
Unité de formation et de recherche de Médecine et Pharmacie, Rouen University, Rouen, France.
Plateau d'Imagerie CardioThoracique de l'Université de Rouen, Rouen, France.
Pharmacology Department, Centre Hospitalier Universitaire de Reims, Reims, France.
Bruker Biospin MRI GMBH, Ettlingen, Germany.
Institut de Recherches Internationales Servier, Suresnes, France.


This study reports preclinical data showing that the interleukin (IL)-1β modulation is a new promising target in the pathophysiological context of heart failure. Indeed, in nondiabetic Wistar and diabetic Goto-Kakizaki rats with chronic heart failure induced by myocardial infarction, administration of the IL-1β antibody gevokizumab improves 'surrogate' markers of survival (i.e., left ventricular remodeling, hemodynamics, and function as well as coronary function). However, whether IL-1β modulation per se or in combination with standard treatments of heart failure improves long-term outcome in human heart failure remains to be determined.


GK, Goto-Kakisaki; I/R, ischemia/reperfusion; IL, interleukin; IL-1β; LV, left ventricle/ventricular; LVEDP, left ventricular end-diastolic pressure; LVEDPV, left ventricular end-diastolic pressure–volume relationship; LVESP, left ventricular end-systolic pressure; LVESPVR, left ventricular end-systolic pressure–volume relationship; ROS, reactive oxygen species; SOD, superoxide dismutase; cardiovascular function; heart failure; ischemia/reperfusion

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