Sentence examples for heart pathogenesis from inspiring English sources

Establishing peptide and protein maps of the Drosophila heart is central to implementation of protein network studies that will allow us to assess the hallmarks of Drosophila heart pathogenesis and gauge the degree of conservation with human disease mechanisms on a systems level.

This article is part of a Special Issue entitled: Heart failure pathogenesis and emerging diagnostic and therapeutic interventions.

Bioactive and biodegradable hydrogels that mimic the extracellular matrix and regulate valve interstitial cells (VIC) behavior are of great interest as three-dimensional (3-D) model systems for understanding mechanisms of valvular heart disease pathogenesis in vitro and the basis for regenerative templates for tissue engineering.

As these epigenetic mechanisms may be altered by the environment and diet, differential DNA methylation may be responsible for integrating environmental/dietary signals and inherited traits to influence heart failure pathogenesis and progression.

Secondly, altered mitochondrial energy metabolism may have had a causal role in heart failure pathogenesis.

Our results provide novel insights about the molecular mechanisms of deregulated miRNA expression during the heart disease pathogenesis.

Here, we review recent evidence regarding the systemic effects of LXRs in relation to co-morbidities that are relevant in heart failure pathogenesis.

The presence of antibodies to calreticulin and to the M1 muscarinic acetycholine receptor, however, has not been investigated in other larger cohorts, and the relevance of the in vitro findings in heart block pathogenesis remains uncertain.

Furthermore, by using hyperpolarized C MR alongside MR-based measurements of cardiac energetics, structure, and contractile function, and in vitro measurements of ATP content and gene/protein expression, we aimed to enhance our understanding of how altered metabolic fluxes contribute to heart failure pathogenesis.

Since LY75 and ADORA2A were not previously known to be involved in DCM or heart failure pathogenesis and both showed significant downregulation in the myocardium of DCM patients, we investigated their functional roles by gene knockdown in zebrafish embryos (Dahme et al, 2009).

It has been well demonstrated that Aβ and tau are at the heart of AD pathogenesis and their interplay in the disease is slowly becoming more evident.