Open AccessThe cancer theory of pulmonary arterial hypertension
Author(s) -
Boucherat Olivier,
Vitry Geraldine,
Trinh Isabelle,
Paulin Roxane,
Provencher Steeve,
Bonnet Sebastien
Publication year - 2017
Publication title -
pulmonary circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.791
H-Index - 40
ISSN - 2045-8940
DOI - 10.1177/2045893217701438
Subject(s) - medicine , hypoxia (environmental) , pulmonary artery , lung cancer , cancer research , cancer cell , cancer , inflammation , pulmonary hypertension , apoptosis , bioinformatics , pathology , immunology , biology , biochemistry , chemistry , organic chemistry , oxygen
Pulmonary arterial hypertension (PAH) remains a mysterious killer that, like cancer, is characterized by tremendous complexity. PAH development occurs under sustained and persistent environmental stress, such as inflammation, shear stress, pseudo‐hypoxia, and more. After inducing an initial death of the endothelial cells, these environmental stresses contribute with time to the development of hyper‐proliferative and apoptotic resistant clone of cells including pulmonary artery smooth muscle cells, fibroblasts, and even pulmonary artery endothelial cells allowing vascular remodeling and PAH development. Molecularly, these cells exhibit many features common to cancer cells offering the opportunity to exploit therapeutic strategies used in cancer to treat PAH. In this review, we outline the signaling pathways and mechanisms described in cancer that drive PAH cells’ survival and proliferation and discuss the therapeutic potential of antineoplastic drugs in PAH.