Chest
The Presence of Genetic Anticipation Suggests That the Molecular Basis of Familial Primary Pulmonary Hypertension May Be Trinucleotide Repeat Expansion
REFERENCE (1)
- et al.
Localization of the gene for familial primary pulmonary hypertension to chromosome 2q31-32 [letter].
Nat Genet
(1997)
Cited by (24)
The -2518A>G promoter polymorphism in the CCL2 gene is not associated with systemic sclerosis susceptibility or phenotype: Results from a multicenter study of European Caucasian patients
2009, Human ImmunologyCitation Excerpt :The roles of CCL2 have been thoroughly investigated and it has found that its biologic activities extend beyond that of chemo-attraction as it can also directly induce cell activation and fibrosis. In this light, CCL2 has been demonstrated to be upregulated in a variety of fibrotic conditions including idiopathic pulmonary fibrosis, systemic sclerosis, and bleomycine-induced experimental scleroderma [1–4]. In addition, the direct role of CCL2 in the fibrotic process has been further substantiated by the observations that CCL2 is able to directly increase type I collagen gene expression by the modulation of TGFβ expression [5], and that mice lacking CCL2 receptor (CCR2) are protected from fluorescein isothiocynate- and bleomycine-induced lung fibrosis [6].
Non-congenital heart disease associated pediatric pulmonary arterial hypertension
2009, Progress in Pediatric CardiologyPulmonary Arterial Hypertension
2006, Vascular Medicine: A Companion to Braunwald's Heart DiseasePulmonary arterial hypertension
2006, Vascular MedicineForeword
2006, Pulmonary Vascular DiseaseThe pathology of pulmonary arterial hypertension
2002, Current Diagnostic Pathology
Supported by National Institutes of Health, National Heart, Lung, and Blood Institute grants HL 48164 and HL 07123.