Overview

Dr. Del Re earned his Ph.D. from the University of California, San Diego. There he trained under Dr. Joan Heller Brown, Chair of
the Department of Pharmacology, investigating the role of the small G-protein RhoA in modulating cardiomyocyte growth and
survival in the context of cardiac ischemic injury.

Dr. Del Re then completed his postdoctoral training in the lab of Dr. Junichi Sadoshima, Chair of Cell Biology and Molecular
Medicine at Rutgers, New Jersey Medical School. As a postdoctoral fellow, Dr. Del Re investigated the role of the Hippo
signaling pathway in the development of heart failure, with a specific focus on upstream regulation of key Hippo pathway
components during myocardial stress.

As Assistant Professor at Rutgers, New Jersey Medical School, Dr. Del Re is interested in elucidating novel signaling pathways
that mediate heart injury, remodeling, and failure following ischemic stress. Projects in the lab focus on Hippo signaling in multiple cardiac cell
types, with the goal of better understanding how the heart responds to stress.

Education

PHD, 2008, University of California, San Diego, La Jolla, CA, Biomedical Sciences
B.S., 2002, Wake Forest Univesity, Winston -Salem, NC, Biology

Relevant Publications

Del Re DP, Amgalan D, Linkermann A, Liu Q, Kitsis RN. Fundamental Mechanisms of Regulated Cell Death and Implications for Heart Disease. Physiol Rev. 2019 Oct 1;99(4):1765-1817.

Francisco J, Byun J, Zhang Y, Kalloo OB, Mizushima W, Oka SI, Zhai P, Sadoshima J, Del Re DP. The tumor suppressor RASSF1A modulates inflammation and injury in the reperfused murine myocardium. J Biol Chem. 2019 Jul 16. pii: jbc.RA119.008970.

Del Re DP. Beyond the Cardiomyocyte: Consideration of HIPPO Pathway Cell-Type Specificity. Circ Res. 2018 Jun 22;123(1):30-32.

Matsuda T, Jeong JI, Ikeda S, Yamamoto T, Gao S, Babu GJ, Zhai P, Del Re DP. H-Ras Isoform Mediates Protection Against Pressure Overload-Induced Cardiac Dysfunction in Part Through Activation of AKT. Circ Heart Fail. 2017 Feb;10(2). pii: e003658.

Matsuda T, Zhai P, Sciarretta S, Zhang Y, Jeong JI, Ikeda S, Park J, Hsu CP, Tian B, Pan D, Sadoshima J, Del Re DP. NF2 Activates Hippo Signaling and Promotes Ischemia/Reperfusion Injury in the Heart. Circ Res. 2016 Aug 19;119(5):596-606.

Del Re DP, Matsuda T, Zhai P, Maejima Y, Jain MR, Liu T, Li H, Hsu CP, and Sadoshima J. Mst1 promotes cardiac myocyte apoptosis through phosphorylation and inhibition of Bcl-xL. Mol. Cell 2014; 54(4): 639-50.

Maejima Y, Kyoi S, Zhai P, Liu T, Li H, Ivessa A, Sciarretta S, Del Re DP, Zablocki DK, Hsu CP, Lim DS, Isobe M and Sadoshima J. Mst1 inhibits autophagy by promoting the interaction between Beclin1 and Bcl-2. Nat. Med. 2013; 19(11):1478-88.

Del Re DP, Yang Y, Nakano N, Cho J, Zhai P, Yamamoto T, Zhang N, Yabuta N, Nojima H, Pan D, Sadoshima J. Yes-associated protein isoform 1 (Yap1) promotes cardiomyocyte survival and growth to protect against myocardial ischemic injury. J Biol Chem. 2013 Feb 8;288(6):3977-88.

Xiang SY, Vanhoutte D, Del Re DP, Purcell NH, Ling H, Banerjee I, Bossuyt J, Lang RA, Zheng Y, Matkovich SJ, Miyamoto S, Molkentin JD, Dorn GW and Brown JH. RhoA protects the mouse heart against ischemia/reperfusion injury. J. Clin. Invest. 2011; 121(8): 3269-76.

Del Re DP, Matsuda T, Zhai P, Gao S, Clark GJ, Van Der Weyden L, and Sadoshima J. Proapoptotic Rassf1A/Mst1 signaling in cardiac fibroblasts is protective against pressure overload in mice. J. Clin. Invest. 2010; 120(10): 3555-67.

Course List

CBNP5155Q		Critical Readings in CBNP
CBNP5000Q		CBNP Thesis Research
CBNP5068Q		Mechanisms of Disease

Molecular mechanisms of heart failure

OVERVIEW
Heart disease is a major health and economic burden worldwide and the leading cause of death in the United States. Although much progress
has been made in understanding the causes of genetic heart disease, ischemic heart disease, and heart failure, the molecular underpinnings
that contribute to injury have yet to be fully elucidated. Unfortunately, the result is current treatments that are largely ineffective.

Our lab aims to better understand the molecular mechanisms responsible for heart injury and the progression to heart failure using a
systems-based approach. Our long-term goal is translating these findings to improved therapeutic approaches for patients.

MECHANISMS of ISCHEMIC HEART INJURY
A major focus of the lab is to understand how the signaling cascade known as the Hippo pathway, a fundamental and conserved growth control
mechanism, influences heart injury, within cardiomyocytes and fibroblasts, as well as in extra-cardiac cell types. Our research group previously
reported that Hippo signaling exhibits cell-type specificity, and can influence paracrine interactions between cardiomyocytes and other cell
types within the heart. We use a combination of complementary approaches including tissue-specific gene targeting, adoptive transfer, and
primary cell culture, to elucidate injury mechanisms that contribute to myocardial infarction.

MECHANISMS of CARDIAC REMODELING and HEART FAILURE
We routinely leverage both ischemic (permanent coronary artery ligation) and non-ischemic (left ventricle pressure overload) stress to model
human pathology, and induce cardiac remodeling and eventual heart failure in mice. Our studies seek to understand the mechanisms that
necessitate cardiac fibrosis, hypertrophy, and decompensation in response to chronic stress, with the goal of identifying novel targets for the
treatment of heart failure.

UNDERSTANDING FUNDAMENTAL PRINCIPLES of INFLAMMATION
We are interested in potential crosstalk between Hippo signaling and innate immune function, both as a basic mechanism of biology, and as it
relates to cardiovascular disease. To this end, we use proteomics and genomics-based approaches in combination with genetically targeted
knockout mice to investigate these pathways.