Unraveling the Cardiac Matrix: From Diabetes to Heart Failure, Exploring Pathways and Potential Medications

• Published in: Biomedicines Vol. 12; no. 6; p. 1314
• Main Authors: Tudurachi, Bogdan-Sorin, Anghel, Larisa, Tudurachi, Andreea, Sascău, Radu Andy, Zanfirescu, Răzvan-Liviu, Stătescu, Cristian
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.06.2024; MDPI
• Subjects: Antidiabetics; Cardiomyocytes; Cardiomyopathy; Cardiovascular diseases; Collagen; Congestive heart failure; Coronary artery disease; Development and progression; Diabetes; Diabetes mellitus (non-insulin dependent); Diabetics; Ejection fraction; Extracellular matrix; Fibroblasts; Fibrosis; GLP-1 agonist; Heart attack; Heart attacks; Heart diseases; Heart failure; Hypertension; Hypoglycemic agents; Identification keys; Inflammation; Ischemia; Mortality; myocardial fibrosis; Myocardial infarction; Prevention; Review; SGLT2 inhibitors; Type 2 diabetes; dipeptidyl peptidase-4 inhibitors; heart failure; GLP-1 agonist; myocardial infarction; diabetes; SGLT2 inhibitors; myocardial fibrosis
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines12061314

Myocardial infarction (MI) often leads to heart failure (HF) through acute or chronic maladaptive remodeling processes. This establishes coronary artery disease (CAD) and HF as significant contributors to cardiovascular illness and death. Therefore, treatment strategies for patients with CAD primarily focus on preventing MI and lessening the impact of HF after an MI event. Myocardial fibrosis, characterized by abnormal extracellular matrix (ECM) deposition, is central to cardiac remodeling. Understanding these processes is key to identifying new treatment targets. Recent studies highlight SGLT2 inhibitors (SGLT2i) and GLP-1 receptor agonists (GLP1-RAs) as favorable options in managing type 2 diabetes due to their low hypoglycemic risk and cardiovascular benefits. This review explores inflammation's role in cardiac fibrosis and evaluates emerging anti-diabetic medications' effectiveness, such as SGLT2i, GLP1-RAs, and dipeptidyl peptidase-4 inhibitors (DPP4i), in preventing fibrosis in patients with diabetes post-acute MI. Recent studies were analyzed to identify effective medications in reducing fibrosis risk in these patients. By addressing these areas, we can advance our understanding of the potential benefits of anti-diabetic medications in reducing cardiac fibrosis post-MI and improve patient outcomes in individuals with diabetes at risk of HF.