Biochemical markers of cardiac remodeling

Abstract

Introduction: Cardiac remodelling is one of the pathogenic pathways leading to heart failure, which occurs due to ischemic, mechanical and inflammatory damage to cardio myocytes and cardiac interstitium. Purpose: Detection of biochemical markers of cardiac remodeling in the context of ischemic myocardial injury. Material and methods: Have been analysed 82 bibliographic sources published during the 2000-2019 in the electronic databases Medline, PubMed, Medscape, Hinari and Google Academic, as well as from the Medical Scientific Library of “Nicolae Testemitanu” State University of Medicine and Pharmacy. Results:The possible mechanisms by which galectin‐3 mediates cardiac fibrosis have been explored by a number of groups (Figure 1). Direct evidence has shown that recombinant galectin‐3 can convert silent fibroblasts into myofibroblasts and induce cardiac fibroblast proliferation, TGF‐β synthesis, collagen production.Was demonstrated that increasing galectin‐3 protein expression by the galectin‐3 gene promotes collagen I synthesis in HL‐I cardiomyocytes, which promotes cardiac decompensation.Others studies revealed that galectin‐3 can promote oxidative stress in human cardiac fibroblasts, a novel mechanism of galectin‐3‐induced cardiac damage. Oxidative stress is a disturbance in the balance between reactive oxygen species (ROS) production and antioxidant detoxification. In patients with HF, oxidative stress occurs in the myocardium and correlates with left ventricular dysfunction. Conclusions: Accumulating studies demonstrate that galectin‐3 is upregulated in clinical and experimental HF and plays an important role in the pathogenesis of cardiac fibrosis. Inhibition of galectin‐3 activation after heart injury may provide an alternative therapeutic approach in the prevention and treatment of HF.