Journal of Diabetology

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Commentary - Journal of Diabetology (2025) Volume 9, Issue 1

Targeting the Heart: Emerging Therapeutic Strategies for Diabetic Cardiomyopathy

Cuthbert Baker*

Department of Community Health Sciences, University of Calgary, Calgary, Alberta, Canada

*Corresponding Author:
Cuthbert Baker
Department of Community Health Sciences
University of Calgary, Calgary, Alberta, Canada
E-mail: cuthbkr@gmail.ca

Received: 01-Mar-2025, Manuscript No. AADY-25-166641; Editor assigned: 03-Mar-2025, PreQC No. AADY-25-166641(PQ); Reviewed: 16-Mar-2025, QC No. AADY-25-166641; Revised: 22-Mar-2025, Manuscript No. AADY-25-166641(R); Published: 25-Mar-2024,DOI:10.35841/aady-9.1.250

Citation: Baker C. Targeting the heart: Emerging therapeutic strategies for diabetic cardiomyopathy. J Diabetol. 2025;9(1):250

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Introduction

Diabetes mellitus affects over 500 million people worldwide and predisposes individuals to various cardiovascular complications, among which diabetic cardiomyopathy (DCM) is a distinct entity marked by myocardial dysfunction. DCM manifests as left ventricular hypertrophy, fibrosis, diastolic dysfunction, and ultimately heart failure, often with preserved ejection fraction initially. Its silent progression and resistance to conventional heart failure treatments necessitate new, targeted approaches to therapy [1].

The pathogenesis of DCM is multifactorial: chronic hyperglycemia induces metabolic shifts favoring fatty acid utilization over glucose, leading to lipotoxicity. Excessive reactive oxygen species (ROS) generation causes oxidative stress, damaging cardiac cells. Chronic inflammation triggers fibrosis through activation of fibroblasts and extracellular matrix deposition. Additionally, mitochondrial dysfunction, impaired calcium handling, and autonomic neuropathy contribute to myocardial dysfunction. This complex interplay presents multiple potential therapeutic targets.

Sodium-glucose cotransporter-2 (SGLT2) inhibitors, initially developed as antidiabetic agents, have demonstrated remarkable cardiovascular benefits independent of glycemic control. Clinical trials (e.g., EMPA-REG OUTCOME, DAPA-HF) reveal reduced hospitalization for heart failure and improved cardiac function. Mechanistically, SGLT2 inhibitors improve myocardial energy metabolism by shifting substrate utilization, reduce inflammation and oxidative stress, and decrease cardiac fibrosis. These effects position SGLT2 inhibitors as a frontline therapy for diabetic patients at risk of or suffering from DCM [2].

Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) also confer cardiovascular protection. They improve endothelial function, reduce oxidative stress, and exhibit anti-inflammatory properties. Some evidence suggests GLP-1 RAs improve left ventricular function and reduce myocardial fibrosis. Their role in DCM is promising but requires further clinical validation.

Therapies targeting cardiac fibrosis are gaining attention. Agents such as pirfenidone, an antifibrotic drug, and inhibitors of transforming growth factor-beta (TGF-β) signaling pathways may mitigate extracellular matrix deposition. Additionally, anti-inflammatory strategies targeting cytokines like interleukin-1 (IL-1) and tumor necrosis factor-alpha (TNF- Mitochondrial dysfunction is central in DCM pathophysiology. Therapeutics aimed at enhancing mitochondrial biogenesis, improving respiratory function, and reducing ROS production are under investigation. Agents like coenzyme Q10, mitochondrial-targeted antioxidants (e.g., MitoQ), and peroxisome proliferator-activated receptor (PPAR) agonists show potential. Optimizing myocardial energy metabolism by promoting glucose oxidation over fatty acid oxidation can also protect cardiac cells [3].

Advancements in gene therapy targeting key molecular pathways implicated in DCM such as antioxidant enzymes or calcium-handling proteins may offer personalized treatments in the future. Stem cell therapy, using mesenchymal stem cells or cardiac progenitors, is being explored for its potential to regenerate damaged myocardium and reduce fibrosis [4].

Lifestyle modifications, including exercise and dietary interventions, remain foundational in managing diabetes and preventing cardiovascular complications. Exercise enhances insulin sensitivity, improves myocardial metabolism, and reduces oxidative stress. Nutritional strategies emphasizing antioxidants and anti-inflammatory foods may complement pharmacotherapy. Emerging data suggest intermittent fasting and ketogenic diets may favorably alter cardiac metabolism in diabetes, though more research is needed.

Despite promising advances, treating DCM remains challenging due to its multifaceted nature and the interplay of systemic and cardiac-specific factors. Early diagnosis is critical but often difficult because symptoms develop late. Biomarkers and advanced imaging techniques are improving detection. Combination therapies targeting multiple pathways simultaneously may prove most effective. Ongoing clinical trials will clarify the roles of novel agents and refine treatment protocols [5].

Conclusion

Diabetic cardiomyopathy poses a significant burden on patients with diabetes, requiring targeted therapeutic strategies beyond glucose control. The advent of SGLT2 inhibitors and GLP-1 receptor agonists has transformed cardiovascular care for diabetic patients, while emerging treatments focusing on fibrosis, inflammation, mitochondrial function, and gene therapy hold great promise. Integrating pharmacological advances with lifestyle interventions offers the best hope for improving cardiac outcomes and quality of life in individuals with diabetic cardiomyopathy.

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