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Medical News: Breakthrough Drug Empagliflozin Shows Promise in Healing Kidney Damage in Diabetics
A groundbreaking study from researchers at multiple top medical institutions in China has revealed that empagliflozin, a drug commonly used to treat diabetes, may offer powerful new hope for people suffering from diabetic kidney disease (DKD). The research team, which included scientists from the Third Affiliated Hospital of Sun Yat-Sen University, Guangdong Provincial People's Hospital, Shunde Hospital of Southern Medical University, and Xunfei Healthcare Technology Co., Ltd., found that empagliflozin does more than just manage blood sugar—it actively reverses kidney fibrosis, a serious complication of diabetes.
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Empagliflozin Found to Reverse Kidney Fibrosis in Diabetic Patients by Blocking Key Enzyme
Kidney fibrosis, or the scarring and thickening of kidney tissue, is a leading cause of kidney failure in diabetic patients. In this Medical News report, it was discovered that empagliflozin works by targeting and lowering the levels of a harmful enzyme called PKM2 in the kidney's tubular cells. High levels of PKM2 were found to accelerate kidney tissue damage and scarring. By reducing PKM2, the drug helps prevent further tissue damage and promotes healing of the kidneys.
How the Study Was Conducted
To assess empagliflozin's effect on kidney fibrosis, the researchers studied both diabetic patients and multiple mouse models with diabetic kidney disease. In the human portion of the study, kidney biopsies were taken from patients either treated with empagliflozin or not. Those receiving the drug showed visibly reduced scarring in kidney tissues, as confirmed by various staining techniques and electron microscope imaging.
In animal experiments, diabetic mice treated with empagliflozin showed clear improvements: lower blood glucose levels, improved body weight, better kidney function, and a reduction in urine protein—a common sign of kidney damage. Most strikingly, the drug dramatically reduced markers of fibrosis and tubular injury in the kidneys of these mice.
The Science Behind Empagliflozin’s Effect
The team used advanced gene sequencing to find out how empagliflozin affects kidney cells at the molecular level. They discovered that the drug significantly lowered the expression of the gene PKM2, which is involved in glycolysis—a process where cells break down glucose for energy. Under diabetic conditions, this enzyme was overly active and linked to increased kidney scarring.
Further lab studies showed that when the PKM2 gene was artificially activated, the beneficial effects of empagliflozin were greatly reduced. This confirms that PKM2 is a key player in driving kidney damage in DKD, and that empagliflozin’s ability to suppress this enzyme is central to its healing properties.
Another major finding was the identification of a transcription factor known as ESRRA that helps turn on the PKM2 gene. Empagliflozin wa
s found to block ESRRA from binding to the PKM2 promoter, thereby shutting down the gene’s activity and halting the chain of damage.
Empagliflozin Also Reduces Cell Changes That Lead to Kidney Scarring
The study also revealed that empagliflozin prevents a damaging cell process known as epithelial-to-mesenchymal transition (EMT). During EMT, kidney tubular cells change form and begin acting like fibroblasts—cells that produce excess collagen and scar tissue. In both human and animal samples, patients treated with empagliflozin showed a reversal of EMT, with healthier cell markers and significantly reduced fibrotic protein production.
Broader Implications for Fatty Liver Disease and Kidney Health
Interestingly, the study also explored how empagliflozin affects mice with both diabetes and fatty liver disease—a common combination in patients with metabolic syndrome. The drug still showed protective effects, reducing kidney fibrosis and restoring healthy enzyme and protein levels even in this more complex disease setting.
Conclusion
This important study sheds new light on how empagliflozin helps diabetic patients not only by lowering blood sugar but by directly reversing the cellular processes that lead to kidney damage and failure. The drug targets the PKM2 enzyme and blocks a harmful gene activation pathway involving ESRRA, stopping fibrosis at its source. These findings could change the way doctors approach the treatment of diabetic kidney disease and offer new hope to millions at risk of kidney failure.
The research proves that empagliflozin is not just a glucose-lowering drug—it is a potential anti-fibrosis therapy that protects and heals kidney tissue. With further studies and clinical trials, empagliflozin could become a cornerstone treatment for preventing kidney failure in diabetics. This breakthrough provides compelling evidence that targeting metabolic pathways within kidney cells may be the future of treating chronic kidney disease in diabetic individuals.
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.researchsquare.com/article/rs-5563608/v1
For the latest on Kidney Fibrosis, keep on logging to Thailand Medical News.
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