Searching for new clues about the molecular cause of endomyocardial fibrosis by way of in silico proteomics and analytical chemistry

Abstract

Endomyocardial Fibrosis (EMF) is a chronic inflammatory disease of the heart with related pathology to that of late stage Chaga’s disease. Indeed, both diseases are thought to result from auto–immune responses against myocardial tissue. As is the case that molecular mimicry between the acidic termini of Trypanosoma cruzi ribosomal P0, P1 and P2â (or simply TcP0, TcP1, and TcP2β) proteins and myocardial tissue causes Chaga’s disease, excessive exposure to certain infections, toxins including cassava ones, allergy and malnutrition has been suggested as the possible cause for EMF. Recent studies have defined the proteomic characteristics of the T. cruzi ribosomal P protein–Ctermini involved in mediating auto–immunity against Beta1–adrenergic receptors of the heart in Chaga’s disease. This study aimed to investigate the similarity of C–termini of TcP0/TcP2β to sequences and molecules of several plants, microbial, viral and chemical elements– most prior thought to be possible causative agents for EMF.