ArticlePloS one2009
Searching for new clues about the molecular cause of endomyocardial fibrosis by way of in silico proteomics and analytical chemistry.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 15 citations in OpenAlex.
- Endomyocardial fibrosis: recent advances and future therapeutic targets.Nature reviews. Cardiology · 2025Review
- From proteome to candidate vaccines: target discovery and molecular dynamics-guided multi-epitope vaccine engineering against kissing bug.Frontiers in immunology · 2024Article
- Core Proteomics and Immunoinformatic Approaches to Design a Multiepitope Reverse Vaccine Candidate against Chagas Disease.Vaccines · 2022Article
- MOGE(S) nosology in low-to-middle-income countries.Nature reviews. Cardiology · 2014Article
- Structural and functional plasticity in long-term cultures of adult ventricular myocytes.Journal of molecular and cellular cardiology · 2013Article
- Microvesicles and intercellular communication in the context of parasitism.Frontiers in cellular and infection microbiology · 2013Review
- Tropical endomyocardial fibrosis in India: a vanishing disease!The Indian journal of medical research · 2012Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundEndomyocardial 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 P2beta (or simply TcP0, TcP1, and TcP2beta) 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-C-termini 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/TcP2beta to sequences and molecules of several plants, microbial, viral and chemical elements- most prior thought to be possible causative agents for EMF. METHODS AND PRINCIPAL
findingsComparative Sequence alignments and phylogeny using the BLAST-P tool at the Swiss Institute of Biotechnology (SIB) revealed homologs of C-termini of TcP0 and TcP2beta among related proteins from several eukaryotes including the animals (Homo sapiens, C. elegans, D. melanogaster), plants (Arabidopsis thaliana, Zea mays, Glycina Max, Oryza sativa, Rhizopus oryzae) and protozoa (P. falciparum, T. gondii, Leishmania spp).The chemical formulae of the two T.cruzi ribosomal protein C-terminal peptides were found to be C(61)H(83)N(13)O(26)S(1)and C(64)H(87)N(13)O(28)S(1) respectively by Protparam. Both peptides are heavily negatively charged. Constitutively, both auto-antigens predominantly contain Asparagine (D), Glycine (G) and Phenylamine (F), with a balanced Leucine (L) and Methionine (M) percent composition of 7.7%. The afore going composition, found to be non-homologous to all molecules of chemical species in the databases searched, suggests the possible role of a metabolic pathway in the pathogenesis of EMF if aligned with our "molecular mimicry" hypothesis.
conclusionsOur findings provide a "window" to suggest that cross reactivity of antibodies against C-terminal sequences of several animal, plant and protozoal ribosomal P proteins with heart tissue may mediate EMF in a similar manner as C- termini of T. cruzi do for Chaga's disease.
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