In patients with type 2 diabetes and chronic kidney disease, finerenone lowers the incidence of major adverse cardiovascular events by 12% compared to placebo, with a similar level of effectiveness...
Mechanism
Synthesis from 1 study
Finerenone works by blocking a harmful hormone signal in the heart and kidneys, which stops swelling and scarring, leading to fewer heart attacks and strokes. Other drugs lower heart risk by different methods — one makes the body get rid of extra fluid and sugar, another improves blood vessel...
Most probable mechanism
A drug blocks a hormone receptor in the heart and kidneys, which stops harmful swelling and scarring in those organs. This reduces pressure on the heart, improves blood flow, and prevents damage that leads to heart attacks, strokes, and heart failure.
A selective nonsteroidal compound binds to mineralocorticoid receptors in renal tubular cells, glomerular cells, and cardiac fibroblasts
Receptor blockade inhibits activation of NF-κB and other pro-inflammatory signaling pathways, reducing production of cytokines such as TNF-α and IL-6
Suppression of fibrotic gene expression decreases deposition of collagen and other extracellular matrix proteins in glomeruli, tubulointerstitium, and myocardium
Reduced renal fibrosis and inflammation restore glomerular filtration barrier integrity, lowering albuminuria and intraglomerular pressure
Decreased cardiac fibrosis improves myocardial compliance, reduces ventricular stiffness, and lowers filling pressures
Improved renal and cardiac structure reduces systemic inflammation, oxidative stress, and neurohormonal activation, decreasing incidence of myocardial infarction, stroke, and cardiovascular death
Less supported by current evidence, but not ruled out
A different drug prevents the kidneys from reabsorbing sugar and salt, causing the body to lose fluid and sodium. This lowers blood volume and pressure, reduces strain on the heart, and improves how heart cells use energy.
Inhibition of sodium-glucose cotransporter 2 in the proximal renal tubule reduces 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 preload, lowering cardiac filling pressures and systemic blood pressure
Reduced hyperglycemia and oxidative stress enhance mitochondrial function and decrease reactive oxygen species production in cardiac and renal tissues
Improved renal hemodynamics and reduced cardiac workload lower the risk of myocardial infarction, stroke, and cardiovascular death
A hormone-like drug binds to receptors on blood vessels and heart cells, making blood vessels relax, reducing inflammation, and helping heart cells survive longer by improving their energy use.
A long-acting GLP-1 analogue binds to GLP-1 receptors on vascular endothelial cells, cardiomyocytes, and macrophages
Receptor activation increases cAMP/PKA signaling, enhancing nitric oxide production and improving endothelial vasodilation
Suppression of macrophage infiltration and reduction in TNF-α and IL-6 levels decrease vascular and myocardial inflammation
Resistance to enzymatic degradation by DPP-4 allows prolonged tissue exposure and sustained signaling compared to shorter-acting analogues
Improved myocardial energetics and reduced apoptosis lower the risk of fatal cardiac events
Evidence from Studies
Supporting (1)
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