Related Experiment Video

Updated: Sep 12, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
09:16

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

7.4K

Canagliflozin Ameliorates Myocardial Fibrosis and Cardiac Function in Chronic Heart Failure: A Dose-Independent

Haomiao Yu1,2, Zhenzhong Han1,2, Wanpeng Chang3

  • 1Department of Endocrinology and Metabology, The First Affiliated Hospital of Shandong First Medical University & Shandong Provincial Qianfoshan Hospital, Jinan, China.

Journal of Cellular and Molecular Medicine
|August 10, 2025
PubMed

Insights

Canagliflozin effectively reduces cardiac fibrosis and improves heart function in chronic heart failure rats. The drug

Area of Science:

  • Cardiology
  • Pharmacology

Background:

  • Myocardial fibrosis drives chronic heart failure progression.
  • Understanding canagliflozin's mechanism against cardiac fibrosis is crucial.

Purpose of the Study:

  • Investigate canagliflozin's effect on cardiac fibrosis in chronic heart failure rats.
  • Determine the dose-dependent efficacy of canagliflozin.

Main Methods:

  • Established chronic heart failure in rats using isoproterenol.
  • Administered canagliflozin (low/high dose) or enalapril for 4 weeks.
  • Assessed cardiac function, fibrosis markers, gene expression (RNA sequencing, qRT-PCR).

Main Results:

  • Canagliflozin improved cardiac function and reduced N-terminal pro-B-type natriuretic peptide.
  • Histological analysis showed reduced collagen deposition and myocardial fibrosis.
  • Canagliflozin inhibited expression of Collagen I, Collagen III, and fibronectin 1.
  • RNA sequencing revealed enrichment in ECM-receptor interaction pathway.
  • Gene expression analysis confirmed reduced levels of fibrosis-related genes.
  • No significant dose-dependent efficacy difference observed between low and high doses.

Conclusions:

  • Canagliflozin directly improves myocardial fibrosis, aiding chronic heart failure management.
  • Canagliflozin's efficacy in this model appears not to be dose-dependent.
Keywords:
Canagliflozinchronic heart failurefibrosis

More Related Videos

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix10:21

Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

Published on: June 14, 2016

10.2K
Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model05:58

Mouse Electroacupuncture Fixation Device Fabrication for Electroacupuncture Pretreatment in Diabetic Cardiomyopathy Mouse Model

Published on: April 18, 2025

293

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...
508
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...
23
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...
722
Heart Failure II: Pathophysiology01:29

Heart Failure II: Pathophysiology

Systolic Heart Failure and Compensatory MechanismsSystolic heart failure (also termed HFrEF, Heart Failure with Reduced Ejection Fraction) is the most prevalent type of heart filure. It results in a decreased volume of blood being pumped from the ventricle. The aortic arch and carotid sinuses have baroreceptors that detect reduced blood pressure, triggering the sympathetic nervous system (SNS) to release epinephrine and norepinephrine. Initially, this response aims to boost heart rate and...
41
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation,...
434
Heart Failure Drugs: Diuretics01:22

Heart Failure Drugs: Diuretics

Heart failure and kidney perfusion are interconnected in a complex way. Reduced renal perfusion and venous congestion are two significant factors that contribute to renal dysfunction in heart failure. The kidneys, primarily responsible for fluid balance in the body, are adversely affected due to compromised cardiac output and increased venous pressure. In response to reduced renal perfusion, the kidneys activate neurohumoral mechanisms to restore balance. However, these mechanisms can be...
484