SGLT2 inhibition reduces cellular senescence in the diabetic kidney by promoting ketone body-induced NRF2 activation https://t.co/XabzTEgIsp
Sodium-glucose cotransporter-2 inhibition reduces cellular senescence in the diabetic kidney by promoting ketone body-induced NRF2 activation.
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Jul 2021 – Nov 2025Where it's discussed
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What people are saying
Discussions reflect a positive reception, with students expressing appreciation for the mechanistic insights, such as the role of ketone bodies and NRF2, using words like 'promising' or 'exciting,' which indicates both engagement and perceived significance of the research. The tone and detailed references suggest users are highly engaged with the scientific content and its potential implications.
Most discussions acknowledge the significance of the findings, with some emphasizing the potential for new treatments.
The topic piqued moderate interest, with comments highlighting the innovative approach and potential benefits.
Comments often include dives into the mechanisms, such as ketone bodies and NRF2 activation, showing active engagement.
Participants seem to believe the research could influence future therapies for diabetic kidney disease, indicating a notable impact.
Abstract in brief
- Dapagliflozin, an SGLT2 inhibitor, reduces cellular aging markers and oxidative stress in diabetic mouse kidneys, demonstrating a protective effect against diabetic kidney disease.
- The drug increases plasma beta-hydroxybutyrate (HB), which helps protect kidney cells by activating NRF2, a key regulator of antioxidant responses, thereby decreasing DNA damage and cell senescence.
- In cell studies, HB and NRF2 activation were shown to reduce aging markers and DNA damage, highlighting a mechanism where ketone bodies promote antioxidant pathways to prevent kidney cell aging in diabetes.]
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SGLT2 inhibition reduces cellular senescence in the diabetic kidney by promoting ketone body-induced NRF2 activation https://t.co/XabzTEgIsp
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