Open AccessPARP inhibition delays transition of hypertensive cardiopathy to heart failure in spontaneously hypertensive rats
Author(s) -
Éva Bartha,
Izabella Solti,
László Kereskai,
János Lantos,
Enikő Plózer,
Klara Magyar,
Eszter Szabados,
Tamás Kálai,
Kálmán Hideg,
Róbert Halmosi,
Balázs Sümegi,
Kálmán Tóth
Publication year - 2009
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvp144
Subject(s) - parp inhibitor , medicine , poly adp ribose polymerase , blood pressure , oxidative stress , endocrinology , heart failure , cardiac function curve , left ventricular hypertrophy , muscle hypertrophy , cardiology , hypertensive heart disease , chemistry , polymerase , gene , biochemistry
Oxidative stress followed by abnormal signalling can play a critical role in the development of long-term, high blood pressure-induced cardiac remodelling in heart failure (HF). Since oxidative stress-induced poly(ADP-ribose)polymerase (PARP) activation and cell death have been observed in several experimental models, we investigated the possibility that inhibition of nuclear PARP improves cardiac performance and delays transition from hypertensive cardiopathy to HF in a spontaneously hypertensive rat (SHR) model of HF.