In patients with type 2 diabetes and chronic kidney disease, finerenone lowers the occurrence of major cardiovascular events by 12% compared to placebo and has a similar effect to SGLT2 inhibitors...
Mechanism
Synthesis from 1 study
A drug blocks a harmful hormone signal in the heart and kidneys, stopping swelling and scarring that can lead to heart attacks and strokes. Other drugs work differently—some reduce blood volume, others improve blood vessel function—but all end up protecting the heart in similar ways.
Most probable mechanism
A drug blocks a hormone receptor in the heart and kidneys, which stops harmful swelling and scarring in blood vessels and heart tissue. This reduces pressure on the heart, improves blood flow, and prevents heart attacks, strokes, and heart-related death.
A selective mineralocorticoid receptor antagonist binds to mineralocorticoid receptors in cardiac fibroblasts, renal tubular cells, and vascular endothelial cells
Receptor blockade inhibits NF-κB and other pro-inflammatory signaling pathways, reducing production of TNF-α, IL-6, and other cytokines in cardiac and renal tissues
Suppression of fibrotic gene expression decreases collagen and extracellular matrix deposition in the myocardium and glomerular basement membrane
Reduced tissue fibrosis improves myocardial compliance and restores glomerular filtration barrier integrity, lowering cardiac filling pressures and systemic vascular resistance
Decreased vascular inflammation and improved endothelial function reduce atherosclerotic plaque instability and thrombotic events
Less supported by current evidence, but not ruled out
A drug blocks glucose reabsorption in the kidneys, causing more salt and water to be excreted. This lowers blood volume and pressure inside the kidney filters, reducing strain on the heart and blood vessels.
Sodium-glucose cotransporter 2 is inhibited in the proximal renal tubule, reducing reabsorption of glucose and sodium
Increased sodium delivery to the macula densa triggers tubuloglomerular feedback, reducing afferent arteriolar pressure and intraglomerular hypertension
Osmotic diuresis and natriuresis decrease plasma volume and venous return, lowering cardiac preload and filling pressures
Reduced hyperglycemia and oxidative stress improve mitochondrial function and decrease reactive oxygen species in vascular and myocardial tissues
A drug activates a receptor on blood vessel and heart cells, improving blood flow and energy use in the heart. The drug lasts longer in the body, allowing continuous protection against damage.
GLP-1 receptor agonists bind to GLP-1 receptors on endothelial cells and cardiomyocytes
Receptor activation increases cAMP/PKA signaling, enhancing nitric oxide production and reducing endothelial dysfunction
Acylated structure confers resistance to enzymatic degradation, enabling sustained tissue exposure and prolonged receptor activation
Reduced macrophage infiltration and suppression of inflammatory mediators improve vascular stability and reduce plaque rupture
Improved myocardial energetics and reduced apoptosis decrease cardiomyocyte loss and preserve cardiac output
Evidence from Studies
Supporting (1)
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Contradicting (0)
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Gold Standard Evidence Needed
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