BME Seminar: Sanjeev G Shroff, PhD
Friday,
November 1, 2019
11:00 AM - 12:00 PM
Department of Computer Science, 500 W. 120th St., New York, New York 10027
Room/Area: 451
Room/Area: 451
All are welcome (attendance required for graduate students). Lunch is provided.
Sanjeev G. Shroff, University of Pittsburgh
RELAXIN: CARDIOVASCULAR ACTIONS AND THERAPEUTIC POTENTIAL
Relaxin, a 6-kDa peptide hormone in the insulin-relaxin superfamily, has important vascular actions that include potent vasodilation and anti-fibrotic effects. The US Food and Drug Administration (FDA) gave relaxin “breakthrough status” in 2013 and Cleveland Clinic named relaxin as one of the Top 10 Medical Innovations for 2014. Much of our knowledge of relaxin has stemmed from investigations of maternal vascular adaptations to pregnancy. With the discovery of local tissue expression and function of relaxin and relaxin receptor in non-pregnant females and males, relaxin has become even more important in the context of the cardiovascular system. This presentation will focus on discussing our relaxin-related work over the past decade, covering basic physiology to potential therapeutic applications: (1) Although our original focus was on relaxin’s vascular actions in the context of pregnancy (Endocrinology 145:3289-3296, 2004; Endocrinology 147:5126-5131, 2006), we made a surprising discovery that relaxin’s vascular actions are not confined to females; males respond equally robustly (J. Appl. Physiol. 98:1013-1020, 2005). Furthermore, relaxin-induced vascular geometric remodeling, and not compositional remodeling, contributes to increased vascular passive compliance under physiological conditions (J. Appl. Physiol. 111: 260-271, 2011; Curr. Hypertens. Rep. 13:409-420, 2011). (2) We provided the first evidence for local relaxin ligand-receptor expression and function in arteries (FASEB J. 20:2352-2362, 2006). (3) We have been examining relaxin’s cardiac actions and therapeutic potential in the context of two pathologies: relaxin-induced left atrial remodeling and suppression of atrial fibrillation (Circ. Res. 113:313-321, 2013) and relaxin-induced left ventricular remodeling and associated functional benefits in the setting of diastolic dysfunction (unpublished data). The cardiovascular actions of relaxin, especially potent systemic and renal vasodilation and potential for improving renal function, were the bases for recent clinical trials (Pre-RELAX-AHF and RELAX-AHF) examining relaxin’s therapeutic efficacy in the setting of acute heart failure.
Sanjeev G. Shroff, University of Pittsburgh
RELAXIN: CARDIOVASCULAR ACTIONS AND THERAPEUTIC POTENTIAL
Relaxin, a 6-kDa peptide hormone in the insulin-relaxin superfamily, has important vascular actions that include potent vasodilation and anti-fibrotic effects. The US Food and Drug Administration (FDA) gave relaxin “breakthrough status” in 2013 and Cleveland Clinic named relaxin as one of the Top 10 Medical Innovations for 2014. Much of our knowledge of relaxin has stemmed from investigations of maternal vascular adaptations to pregnancy. With the discovery of local tissue expression and function of relaxin and relaxin receptor in non-pregnant females and males, relaxin has become even more important in the context of the cardiovascular system. This presentation will focus on discussing our relaxin-related work over the past decade, covering basic physiology to potential therapeutic applications: (1) Although our original focus was on relaxin’s vascular actions in the context of pregnancy (Endocrinology 145:3289-3296, 2004; Endocrinology 147:5126-5131, 2006), we made a surprising discovery that relaxin’s vascular actions are not confined to females; males respond equally robustly (J. Appl. Physiol. 98:1013-1020, 2005). Furthermore, relaxin-induced vascular geometric remodeling, and not compositional remodeling, contributes to increased vascular passive compliance under physiological conditions (J. Appl. Physiol. 111: 260-271, 2011; Curr. Hypertens. Rep. 13:409-420, 2011). (2) We provided the first evidence for local relaxin ligand-receptor expression and function in arteries (FASEB J. 20:2352-2362, 2006). (3) We have been examining relaxin’s cardiac actions and therapeutic potential in the context of two pathologies: relaxin-induced left atrial remodeling and suppression of atrial fibrillation (Circ. Res. 113:313-321, 2013) and relaxin-induced left ventricular remodeling and associated functional benefits in the setting of diastolic dysfunction (unpublished data). The cardiovascular actions of relaxin, especially potent systemic and renal vasodilation and potential for improving renal function, were the bases for recent clinical trials (Pre-RELAX-AHF and RELAX-AHF) examining relaxin’s therapeutic efficacy in the setting of acute heart failure.
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