Overexpression of collagen type III in injured myocardium prevents cardiac systolic dysfunction by changing the balance of collagen distribution

Abstract

Overexpression of Col3 improved cardiac function by changing the balance of collagen distribution in LV remodeling. The SVVYGLR motif of the thrombin-cleaved N-OPN and SV peptide attenuated cardiac dysfunction by increasing Col3 and changing the pattern of collagen balance in the impaired area.

LncRNA-MIAT-Mediated miR-214-3p Silencing Is Responsible for IL-17 Production and Cardiac Fibrosis in Diabetic Cardiomyopathy

“…Cardiovascular complications are one of the most leading cause of morbidity and mortality in diabetic patients (Uchinaka et al, 2018). The mechanism of DCM is complex, which involves a diversity of pathophysiological changes that include increased oxidative/nitrative stress, activation of various proinflammatory and cell death pathways (De Gonzalo-Calvo et al, 2016;Chen et al, 2019).…”

“…Moreover, the production can be rescued after AMO-miR-214-3p application (Figure 4E). It is well-documented that the expression of cardiac collagen types I and III is highly associated with cardiac fibrosis, and severe fibrosis impairs cardiac contractility (Uchinaka et al, 2018). Therefore, we next performed confocal immunochemical staining of collagen I and collagen III to determine if HG induces cardiac fibrosis via elevation of collagen I and III.…”

Think beyond the cell: Can we [tissue] engineer a solution to heart failure?

“…The strength of this work is consistency, a hypothesis withstanding both direct application of Col3-secreting fibroblast sheets as well as the administration of the functional motif of N-terminal osteopontin fragment. For their modest group sizes, the consistency in the findings of Uchinaka and colleagues 6 is relatively impressive, both in their histologic findings and in serial echocardiographic measurements, such that they were able to detect statistical significance in minor differences in cardiac function. Their values remain logical across all time points, possibly hinting at some longitudinal benefits of Col3 overexpression that extend well beyond the initial therapeutic period, delineating a narrative of efficacy that supports the initial hypothesis.…”

“…The article by Uchinaka and colleagues 6 in this issue of the Journal comes at this opportune junction. Their experimental design was predicated on our understanding of myocardial contractility and extracellular matrix composition, namely the protective role of collagen type III (Col3) relative to collagen type I in both systolic and diastolic function after infarction and in tissue viscoelasticity.…”

“…Their values remain logical across all time points, possibly hinting at some longitudinal benefits of Col3 overexpression that extend well beyond the initial therapeutic period, delineating a narrative of efficacy that supports the initial hypothesis. There is strength in correlation of functional and immunohistologic evidence, with Uchinaka and colleagues 6 noting increased distribution of Col3 in the treatment group and reduced scar size correlating with reduced eccentric cardiac remodeling, as evidenced by left ventricular chamber diameter, ejection fraction, and fractional shortening.…”