Work

Pressure overload induces IL-18 and IL-18R expression, but markedly suppresses IL-18BP expression in a rabbit model. IL-18 potentiates TNF-α-induced cardiomyocyte death

Year: 2014

Type: article

Source: Journal of Molecular and Cellular Cardiology

DOI: 10.1016/j.yjmcc.2014.07.007

Authors: Tadashi Yoshida, Ingeborg Friehs, Srinivas Mummidi, Pedro J. del Nido, Solange Addulnour-Nakhoul, Patrice Delafontaine, Anthony J. Valente, Bysani Chandrasekar

Institutions: Tulane University, Boston Children's Hospital, Harvard University, The University of Texas at San Antonio Health Science Center, South Texas Veterans Health Care System, Southeast Louisiana Veterans Health Care System

Language: English

Topic: Cardiac Fibrosis and Remodeling

Subfield: Cardiology and Cardiovascular Medicine

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: green

Funders: U.S. Department of Veterans Affairs, Office of Research and Development, National Heart, Lung, and Blood Institute, National Institute of General Medical Sciences

Awards: G1055511557, The Role of Interleukin-18 in Myocardial Hypertrophy and Failure, G171332315, Myocardial Hypertrophy and Therapeutic Angiogenesis, G2377109628, G3682146654, G4305893308, Mentoring Research Excellence in Aging and Regenerative Medicine, G5629502726, G6271339468, G693365333, ANGIOTENSIN II, IGF-1 AND SKELETAL MUSCLE ATROPHY, Insulin-Like Growth Factor-1 and Atherosclerosis

OpenAlex ID: W2002982022

FWCI: 2.058

Cites: 41

Cited by: 46

Related to: 10