Galectin-3 Inhibition Ameliorates Streptozotocin-Induced Diabetic Cardiomyopathy in Mice

Zhu, Ning; Zhu, Liuyan; Huang, Bifei; Xiang, Wei; Zhao, Xuyong

doi:10.3389/fcvm.2022.868372

Cited by 8 publications

(9 citation statements)

References 68 publications

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“…Gal-3 KO mice showed less hyperglycemia and less pancreatic injury after STZ due to reduced inflammation ( Mensah-Brown et al, 2009 ), but Gal-3 overexpression in pancreatic b cells led to reduced apoptosis and resistance to STZ damage ( Jovicic et al, 2021 ). Regarding DCMP and Gal-3, results are more consistent: Gal-3 KO mice had less myocardial injury, better remodeling and cardiac function, and less interstitial fibrosis ( Zhu et al, 2022 ). This protective effect was mediated by reduced oxidative stress and apoptosis.…”

Section: Galectin-3 In Cardiovascular Diseasementioning

confidence: 86%

Unraveling the role of galectin-3 in cardiac pathology and physiology

Seropian,

Cassaglia,

Miksztowicz

et al. 2023

Front. Physiol.

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Galectin-3 (Gal-3) is a carbohydrate-binding protein with multiple functions. Gal-3 regulates cell growth, proliferation, and apoptosis by orchestrating cell-cell and cell-matrix interactions. It is implicated in the development and progression of cardiovascular disease, and its expression is increased in patients with heart failure. In atherosclerosis, Gal-3 promotes monocyte recruitment to the arterial wall boosting inflammation and atheroma. In acute myocardial infarction (AMI), the expression of Gal-3 increases in infarcted and remote zones from the beginning of AMI, and plays a critical role in macrophage infiltration, differentiation to M1 phenotype, inflammation and interstitial fibrosis through collagen synthesis. Genetic deficiency of Gal-3 delays wound healing, impairs cardiac remodeling and function after AMI. On the contrary, Gal-3 deficiency shows opposite results with improved remodeling and function in other cardiomyopathies and in hypertension. Pharmacologic inhibition with non-selective inhibitors is also protective in cardiac disease. Finally, we recently showed that Gal-3 participates in normal aging. However, genetic absence of Gal-3 in aged mice exacerbates pathological hypertrophy and increases fibrosis, as opposed to reduced fibrosis shown in cardiac disease. Despite some gaps in understanding its precise mechanisms of action, Gal-3 represents a potential therapeutic target for the treatment of cardiovascular diseases and the management of cardiac aging. In this review, we summarize the current knowledge regarding the role of Gal-3 in the pathophysiology of heart failure, atherosclerosis, hypertension, myocarditis, and ischemic heart disease. Furthermore, we describe the physiological role of Gal-3 in cardiac aging.

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Section: Galectin-3 In Cardiovascular Diseasementioning

confidence: 86%

Unraveling the role of galectin-3 in cardiac pathology and physiology

Seropian,

Cassaglia,

Miksztowicz

et al. 2023

Front. Physiol.

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“…Intervening in the response to histone methylation‐induced inflammation is also one of the strategies 73 Galangin. can ameliorate DCM by reducing oxidative stress and inflammation 74,75 . Hao et al.…”

Section: Protein Methylation In Diabetic Cardiomyopathymentioning

confidence: 99%

“… 73 Galangin can ameliorate DCM by reducing oxidative stress and inflammation. 74 , 75 Hao et al. proposed that DNA methylation and histone modifications may play an important role in microvascular complications of DCM and thereby represent a potential therapeutic target.…”

Section: Protein Methylation In Diabetic Cardiomyopathymentioning

confidence: 99%

Post‐translational modifications in diabetic cardiomyopathy

Li,

Chen,

Huang

et al. 2024

J Cellular Molecular Medi

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The increasing attention towards diabetic cardiomyopathy as a distinctive complication of diabetes mellitus has highlighted the need for standardized diagnostic criteria and targeted treatment approaches in clinical practice. Ongoing research is gradually unravelling the pathogenesis of diabetic cardiomyopathy, with a particular emphasis on investigating various post‐translational modifications. These modifications dynamically regulate protein function in response to changes in the internal and external environment, and their disturbance of homeostasis holds significant relevance for the development of chronic ailments. This review provides a comprehensive overview of the common post‐translational modifications involved in the initiation and progression of diabetic cardiomyopathy, including O‐GlcNAcylation, phosphorylation, methylation, acetylation and ubiquitination. Additionally, the review discusses drug development strategies for targeting key post‐translational modification targets, such as agonists, inhibitors and PROTAC (proteolysis targeting chimaera) technology that targets E3 ubiquitin ligases.

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“…Reducing ventricular dilation, congestion, and fibrosis through the suppression of Gal-3 mRNA expression in Mst1-TG mice, which model DCM with high levels of cardiac Gal-3, is a promising therapeutic approach [ 109 ]. Silencing Gal-3 reduces myocardial dysfunction in DCM animals by downregulation of macrophage infiltration and inflammatory cytokine release triggered by HG via the Gal-3/NF-κB p65 regulatory network in STZ-induced DCM in mice [ 110 ]. Taking into account the foregoing, it seems reasonable to conclude that Gal-3 can be used as a prognostic marker for heart failure and is also well indicated in diabetic myocardium and that inhibition of Gal-3 to reduce inflammation and fibrosis is a potential therapeutic approach to prevent heart disease.…”

Section: Mechanisms Contributing To the Development Of Dcmmentioning

confidence: 99%

Potential clinical biomarkers and perspectives in diabetic cardiomyopathy

Deng

Fang

Tian

et al. 2023

Diabetol Metab Syndr

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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.

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Galectin-3 Inhibition Ameliorates Streptozotocin-Induced Diabetic Cardiomyopathy in Mice

Abstract: Graphical AbstractGal-3 triggers myocardial apoptosis, oxidative stress, inflammatory cytokines release, macrophage infiltration, and fibrosis, leading to cardiac dysfunction in DCM mice.

Cited by 8 publications

References 68 publications

Unraveling the role of galectin-3 in cardiac pathology and physiology

Unraveling the role of galectin-3 in cardiac pathology and physiology

Post‐translational modifications in diabetic cardiomyopathy

Potential clinical biomarkers and perspectives in diabetic cardiomyopathy

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