Potential clinical biomarkers and perspectives in diabetic cardiomyopathy

Abstract

Diabetic cardiomyopathy (DCM) is a serious cardiovascular complication and the leading cause of death in diabetic patients. Patients typically do not experience any symptoms and have normal systolic and diastolic cardiac functions in the early stages of DCM. Because the majority of cardiac tissue has already been destroyed by the time DCM is detected, research must be conducted on biomarkers for early DCM, early diagnosis of DCM patients, and early symptomatic management to minimize mortality rates among DCM patients. Most of the existing implemented clinical markers are not very specific for DCM, especially in the early stages of DCM. Recent studies have shown that a number of new novel markers, such as galactin-3 (Gal-3), adiponectin (APN), and irisin, have significant changes in the clinical course of the various stages of DCM, suggesting that we may have a positive effect on the identification of DCM. As a summary of the current state of knowledge regarding DCM biomarkers, this review aims to inspire new ideas for identifying clinical markers and related pathophysiologic mechanisms that could be used in the early diagnosis and treatment of DCM.

Esculeoside A Decreases Diabetic Cardiomyopathy in Streptozotocin-Treated Rats by Attenuating Oxidative Stress, Inflammation, Fibrosis, and Apoptosis: Impressive Role of Nrf2

“…It can also facilitate the progression of HF in diabetic hearts by promoting lipotoxicity and the generation of ROS [40]. ANP and BNP are two major HF markers released into the serum from the hypertrophied cardiac wall stain [41,42]. In addition, LDH, CK-MB, and TPI are important markers for assessing cardiomyocyte injury, as they are released from the damaged cardiomyocytes and are markers of cell membrane disintegration [43].…”

Diabetic cardiomyopathy: Early diagnostic biomarkers, pathogenetic mechanisms, and therapeutic interventions

“…The detection of serum markers, such as increased inflammatory mediators (TNFα, isoprostanes, IL-6, and C-reactive protein), elevated fibrotic markers (TGFβ1 and IGFBP7) and decreased antioxidant markers (leptin, adiponectin, and bilirubin), can also provide a basis for the early diagnosis and treatment of DCM [ 12 ]. Recent studies have shown that a number of new novel markers, such as galactin-3 (Gal-3), adiponectin (APN), and irisin, are significantly changed in the clinical course of the various stages of DCM [ 13 ]. Moreover, evidence suggests that exosomes, microRNAs, and long noncoding RNAs have potential applications as biomarkers for the detection of DCM [ 14 , 15 ].…”

Multi-omics analysis reveals attenuation of cellular stress by empagliflozin in high glucose-treated human cardiomyocytes

“…Diabetic cardiomyopathy (DCM) is a common cardiovascular complication in diabetic patients characterized by fibrosis, stiffness, and hypertrophy that induce adverse cardiac structure and performance with consequent diastolic and systolic dysfunction [ 1 ]. In severe conditions, DCM can evolve into heart failure, an alteration of cardiac structure/function, inducing an inadequate cardiac output, and an increased left ventricular filling pressure [ 2 , 3 ].…”

“…In severe conditions, DCM can evolve into heart failure, an alteration of cardiac structure/function, inducing an inadequate cardiac output, and an increased left ventricular filling pressure [ 2 , 3 ]. The DCM pathophysiology has been well-studied, and several mechanisms have been demonstrated to clarify how diabetes promotes cellular dysfunction [ 1 , 4 ]. Specifically, the high glucose levels enhance the production of advanced glycation end products (AGEs), leading to cardiovascular injury via crosslinking of extracellular matrix molecules [ 5 ].…”