Key result
Targeting oxidative stress and inflammation with SGLT2i, GLP-1RAs, or vericiguat may mitigate hypertension-mediated organ damage.
Why the study?
To describe the pathophysiological mechanisms associated with cardiac hypertrophy and discuss recent innovative therapeutic strategies targeting these molecular pathways to prevent and manage hypertension-mediated organ damage.
Novel agents such as SGLT2 inhibitors, GLP-1 receptor agonists, and vericiguat offer promising therapeutic avenues to prevent and manage hypertension-mediated cardiac hypertrophy by directly targeting oxidative stress, mitochondrial dysfunction, and inflammatory pathways.
Cardiac hypertrophy represents a central manifestation of hypertension-mediated organ damage (HMOD), which consists of structural and functional changes as a response to sustained pressure overload. Oxidative stress and inflammation play central roles in the development of cardiac hypertrophy, contributing to myocardial remodeling in association with mechanical stress and neurohormonal activation. The imbalance between the production of reactive oxygen species and antioxidant defense mechanisms is associated with the activation of signaling pathways and the expression of genes involved in the development and progression of cardiac fibrosis and hypertrophy. Oxidative stress is also related to mitochondrial dysfunction, redox-sensitive transcription factors, post-translational modifications, and epigenetic modulation. Novel therapeutic strategies can target these molecular pathways, reducing the impact of hypertension on HMOD. Type-2 sodium glucose transporter inhibitors were shown to restore mitochondrial bioenergetics, reducing oxidative stress, and suppressing inflammation. Also, glucagon-like peptide-1 receptor agonists reduce ROS generation and stabilize mitochondrial structure and function. In addition, vericiguat, which represents an approach targeted to restore nitric oxide-soluble guanylate cyclase signaling, might represent a valuable therapeutic approach, working to prevent and slow the progression of cardiac hypertrophy before the development of heart failure. In this review we will describe the pathophysiological mechanisms associated with cardiac hypertrophy and discuss the recent innovative therapeutic strategies with potential implications for prevention and management.
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Gallo et al. (2025) conducted a review in Hypertension-mediated organ damage and cardiac hypertrophy. Targeted molecular therapies (SGLT2 inhibitors, GLP-1 receptor agonists, vericiguat) was evaluated. Oxidative stress, mitochondrial dysfunction, and inflammation drive hypertension-mediated organ damage, offering novel therapeutic targets for SGLT2 inhibitors, GLP-1RAs, and vericiguat.
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