Related Experiment Video

Updated: Jun 27, 2026

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model
03:45

Investigating the Pathogenesis of MYH7 Mutation Gly823Glu in Familial Hypertrophic Cardiomyopathy using a Mouse Model

Published on: August 8, 2022

SGLT2 Inhibitors in Hypertrophic Cardiomyopathy: Emerging Evidence and Putative Mechanisms

Khrystyna Ryabenko1,2, Valérie Schini-Kerth3, Patrick Ohlmann3,4

  • 1Cardiology Unit, Cardiac Thoracic and Vascular Department, IRCCS Azienda Ospedaliera-Universitaria di Bologna, 40138 Bologna, Italy.

Biomolecules
|June 26, 2026
PubMed

Insights

Hypertrophic cardiomyopathy (HCM) involves oxidative stress and mitochondrial issues. Sodium-glucose cotransporter 2 inhibitors (SGLT2i) show promise in treating HCM by targeting these pathways.

Area of Science:

  • Cardiology
  • Molecular Medicine
  • Metabolic Disorders

Background:

  • Hypertrophic cardiomyopathy (HCM) is a primary inherited heart muscle disease linked to heart failure and sudden cardiac death.
  • While genetic mutations initiate HCM, oxidative stress, mitochondrial dysfunction, and nutrient signaling significantly drive its progression.
  • Reactive oxygen species (ROS) exacerbate HCM by impairing energy production, calcium handling, and promoting fibrosis.

Purpose of the Study:

  • To review the molecular mechanisms linking oxidative stress and hypertrophic remodeling in HCM.
  • To explore the potential of sodium-glucose cotransporter 2 inhibitors (SGLT2i) as a disease-modifying therapy for HCM.

Main Methods:

  • Literature review of preclinical and translational studies on HCM.
  • Analysis of the role of oxidative stress and mitochondrial dysfunction in HCM pathogenesis.
  • Evaluation of the therapeutic mechanisms of SGLT2 inhibitors in cardiovascular disease.

Main Results:

  • SGLT2 inhibitors demonstrate cardioprotective effects in heart failure, independent of glucose control.
  • SGLT2i improve myocardial metabolism, reduce oxidative stress, and enhance mitochondrial function.
  • Preclinical data suggest SGLT2i may counteract key pathophysiological processes in HCM.

Conclusions:

  • Oxidative stress and mitochondrial dysfunction are critical in HCM progression.
  • SGLT2 inhibitors possess pleiotropic effects that may counteract HCM pathophysiology.
  • Targeting these mechanisms with SGLT2 inhibitors represents a potential disease-modifying strategy for HCM.

Keywords:
gliflozineshypertrophic cardiomyopathyinflammationreactive oxygen speciessodium–glucose cotransporter 2 inhibitors

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
Cardiomyopathy III: Hypertrophic Cardiomyopathy01:29

Cardiomyopathy III: Hypertrophic Cardiomyopathy

Hypertrophic cardiomyopathy, or HCM, is an autosomal dominant genetic disorder characterized by asymmetric left ventricular hypertrophy without ventricular dilation. It is more common in men and is typically diagnosed in young, athletic adults.EtiologyHCM is primarily genetic and is caused by mutations in genes encoding sarcomeric proteins. Researchers have identified over 1400 mutations across at least 11 different genes. Among these, the most frequently occurring mutations are found in the...
Cardiomyopathy V: Interprofessional Care01:29

Cardiomyopathy V: Interprofessional Care

Managing cardiomyopathy involves addressing underlying or precipitating causes, treating heart failure with medications, and implementing dietary changes and a balanced exercise and rest regimen.Lifestyle ModificationsCardiomyopathy patients should adopt a low-sodium diet to reduce fluid retention and manage heart failure. A personalized exercise and rest plan helps maintain physical fitness without overstraining the heart. Avoiding alcohol and tobacco is essential to prevent further damage to...
Heart Failure Drugs: Inotropic Agents01:26

Heart Failure Drugs: Inotropic Agents

Positive inotropic agents are commonly used as the first line of treatment for heart failure. One such agent is digoxin, derived from the genus Digitalis, which has been known for centuries but effectively utilized since 1785. However, these cardiac glycosides can have potentially toxic effects due to their mechanism of action, which involves inhibiting Na+/K+-ATPase and increasing contractility. Digoxin is absorbed orally and distributed in various tissues, including the CNS. It has a long...
Heart Failure V: Medical Management01:30

Heart Failure V: Medical Management

Medical Management of Acute Decompensated Heart Failure (ADHF)The primary goals of therapy for patients hospitalized with acute decompensated heart failure (ADHF) include:Relieving symptomsOptimizing volume statusSupporting oxygenation and ventilationMaintaining cardiac output (CO) and end-organ perfusionIdentifying and addressing the cause of ADHFPreventing complicationsProviding patient education on factors precipitating HF exacerbationPlanning for dischargeOngoing monitoring and assessment...
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include: