A physiologist from Belarus who's worked at the Medical University of South Carolina for almost 10 years thinks she's found a mechanism that could explain why.
"Pulmonary fibrosis is a deadly, very complex disease where the lung's air sacs are replaced by tough fibrotic tissue," Galina Bogatkevich said. Using modern physiological technology called proteomics, Bogatkevich's laboratory compared healthy and diseased lung fluid and found that a key growth factor that is supposed to inhibit fibrotic growth is malfunctioning.
"This is the first time we've identified a physiological difference that parallels the profound differences between black and whites in the severity of the disease and prognosis," she said in an American Physiological Society session at Experimental Biology in San Francisco.
*Paper presentation: "Antifibrotic effect of hepatocyte growth factor is impaired in lung fibroblasts isolated from African-Americans," APS Physiology Airway Mechanics and Mechanotransduction in the Lung 767.9/board #C684. Research was by Galina Stephanie Bogatkevich, Anna Ludwicka-Bradley, D. Beth Singleton and Richard M. Silver, Department of Medicine, Medical University of South Carolina, Charleston.
Proteomic approach finds lowered antifibrotic HGF among black patients
Pulmonary fibrosis (PF) strikes nine of out 10 patients with systemic sclerosis or scleroderma, a group of diseases involving abnormal growth of the connective tissue that supports the skin and internal organs. Current thinking is that pulmonary fibrosis is caused by micro injury to the lung as part of the earlier diseases' progress.
"But we also know that PF is a 'proteomic disease' that is its pathogenesis depends on the imbalance in expression and communicati