Related Experiment Video

Updated: Aug 1, 2025

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
08:15

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease

Published on: May 10, 2024

616

[Mineralocorticoid receptor antagonists: A new therapeutic option for diabetic kidney disease]

Sophie Girerd1, Matthieu Soulie2, Jonatan Barrera-Chimal3

  • 1Département de néphrologie, CHRU de Nancy, Nancy, France - Centre d'investigation clinique-plurithématique (CIC-P) 1433, F-CRIN INI-CRCT - Essais cliniques cardiovasculaires et rénaux, CHRU de Nancy, Nancy, France - Inserm U1116, université de Lorraine, France.

Medecine Sciences : M/S
|April 24, 2023
PubMed

Insights

Mineralocorticoid receptor (MR) antagonists, like finerenone, show significant benefits for cardiorenal outcomes in diabetic kidney disease (DKD). These findings highlight a new therapeutic avenue for managing DKD complications.

Area of Science:

  • Endocrinology and Nephrology
  • Cardiovascular Medicine

Context:

  • Diabetic kidney disease (DKD) is a major complication of diabetes, leading to significant cardiovascular morbidity.
  • Mineralocorticoid receptor (MR) activation contributes to DKD pathophysiology through inflammatory and fibrotic pathways.

Purpose:

  • To summarize the role of MR activation in DKD.
  • To review clinical trial data on finerenone for DKD.
  • To discuss finerenone's place in DKD therapy.

Summary:

  • Experimental studies suggest MR antagonists benefit cardiorenal outcomes in kidney disease models.
  • The FIDELIO-DKD and FIGARO-DKD trials demonstrated finerenone's efficacy in improving renal and cardiac outcomes in DKD patients.
  • Finerenone, a non-steroidal MR antagonist, offers a novel therapeutic option for DKD.

Impact:

  • Provides evidence for finerenone as a treatment for DKD, potentially reducing cardiovascular events and kidney disease progression.
  • Highlights the importance of targeting the MR pathway in managing diabetic complications.
  • Informs clinical practice regarding therapeutic strategies for diabetic kidney disease.

More Related Videos

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice10:31

Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice

Published on: May 2, 2025

241
Delivery of Exogenous Artificially Synthesized miRNA Mimic to the Kidney Using Polyethylenimine Nanoparticles in Several Kidney Disease Mouse Models07:01

Delivery of Exogenous Artificially Synthesized miRNA Mimic to the Kidney Using Polyethylenimine Nanoparticles in Several Kidney Disease Mouse Models

Published on: May 10, 2022

1.6K

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...
474
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...
433
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
662
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
721
Antihypertensive Drugs: Action of Diuretics01:16

Antihypertensive Drugs: Action of Diuretics

Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various...
825
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
794