Pulmonary hypertension in adult Alk1 heterozygous mice due to oxidative stress
Author(s) -
Mirjana Jerkić,
Mohammed G. Kabir,
Adrienne Davies,
Lisa Yu,
Brendan A.S. McIntyre,
Nasir W. Husain,
Masahiro Enomoto,
Valentin Sotov,
Mansoor Husain,
Mark Henkelman,
Jaques Belik,
Michelle Letarte
Publication year - 2011
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/cvr232
Subject(s) - medicine , endocrinology , pulmonary hypertension , oxidative stress , reactive oxygen species , enos , endothelial dysfunction , lung , nitric oxide , biology , nitric oxide synthase , biochemistry
Mutations in the ALK1 gene, coding for an endothelial-specific receptor of the transforming growth factor-β superfamily, are the underlying cause of hereditary haemorrhagic telangiectasia type 2, but are also associated with familial pulmonary hypertension (PH). We assessed the lung vasculature of mice with a heterozygous deletion of Alk1 (Alk1(+/-)) for disease manifestations and levels of reactive O(2) species (ROS) implicated in both disorders.
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