Endothelial cell modulation of cardiomyocyte gene expression

Abstract

WB Western blot WGA Wheat germ agglutinin β-MHC -Myosin heavy chain 2013, Fredriksen et al., 2001). Kidney disease is commonly found in heart failure (HF) patients (Grande et al., 2017). It was found that GFR is associated with the degree of cardiac diastolic dysfunction and adverse clinical outcomes (Jain et al., 2017). A recent nationwide population-based cohort study showed that heart failure patients have a higher risk of developing dementia (Adelborg et al., 2017). Studies also revealed post-mortem that 73.6% ± 7.0% of all cardiomyocytes were mono-nucleated, 25.5% ± 7.4% were bi-nucleated, and 1.0% ± 1.2% were tri-nucleated in the heart of individuals aged one month to 73 years. In agreement with previous studies (Mollova et al., 2013, Olivetti et al., 1996), they established that already 1 month after birth; the final number of cardiomyocytes was reached (3.2 ± 0.75 × 10 9 cells) and remained constant throughout life. By stereological measuring the average volume of cardiomyocytes at different ages, it was found that the adaptive about 3-fold greater (endothelium-derived contracting factors) (Flammer et al., 2012). Furchgott and Zawadzki (Furchgott and Zawadzki, 1980) first described the phenomenon of endothelium-dependent relaxation in 1980. Subsequently, the identification of nitric oxide (NO) as the crucial endothelium-derived mediator of vascular relaxation led to substantial progress in cardiovascular research (Flammer et al., 2012). In addition to with arterial hypertension and echocardiographically documented left ventricular hypertrophy, who received either the AT 1 receptor blocker losartan or the β 1 receptor blocker atenolol, were much less likely to experience such a major cardiovascular event (Kjeldsen et al., 2002). Also whereby NT-proBNP levels are more sensitive and specific to distinguish HF from non-HF subjects (Fonseca et al., 2004). NT-proBNP levels were also suggested to be highly predictive of incident atrial fibrillation, the most common cardiac rhythm abnormality, after adjustment for an extensive number of covariates (Patton et al., 2009). Although ANP and BNP have been recommended to provide prognostic information

<p>Sirt6-Mediated Endothelial-to-Mesenchymal Transition Contributes Toward Diabetic Cardiomyopathy via the Notch1 Signaling Pathway</p>

“…As reviewed in the introduction, EndMT is an important cellular phenomenon that induces microvascular dysfunction and acts as an important source of myofibroblasts that directly affect cardiac function in DCM. 23,24 EndMT has also been implicated in the pathogenesis of diabetic fibrosis; for instance, Wang et al reported that HG levels can induce EndMT in human umbilical vein endothelial cells, including changes in corresponding protein expression and morphology. 25 These evidences indicate the sensitivity of endothelial cells to hyperglycemia, but there was no direct evidence to support the EndMT in CMECs caused by T2DM.…”

The origin, progress, and application of cell‐based cardiac regeneration therapy

“…In addition, ECs can also synthesize and secrete a variety of bioactive cytokines. This endothelial paracrine activity, known as endothelial microenvironment function, is important for organ maintenance and tissue repair and regeneration (He et al, 2017; Jiang et al, 2019; Kivela et al, 2019).…”

Endothelial cell dysfunction in cardiac disease: driver or consequence?

“…For example, EC have been shown to protect cocultured CM from hypoxia-reoxygenation injury via both hypoxia-inducible factor (HIF1α) ( Leucker et al, 2011 ) and NO signaling ( Leucker et al, 2013 ). Similarly, transwell coculture systems have implicated EC-derived paracrine factors in control of CM cytoskeletal organization ( Zhang et al, 2015 ) and natriuretic peptide expression ( Jiang et al, 2019 ).…”