ArticleJournal of cellular and molecular medicine2024
SGLT2i improves kidney senescence by down-regulating the expression of LTBP2 in SAMP8 mice.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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6 citing papers in PubMed, 8 citations in OpenAlex.
- Mechanistic Links Between the Gut Microbiome and Longevity Therapeutics.Biomedicines · 2026Review
- The Effects of SNPs in theVeterinary medicine international · 2026Article
- Multi-target regulation of cellular senescence by traditional Chinese medicine: a novel strategy to preventing diabetic kidney disease.Renal failure · 2025Review
- SGLT2 inhibitors as a novel senotherapeutic approach.npj aging · 2025Review
- Sodium-dependent glucose transporter 2 inhibitors: Transforming diabetic cardiomyopathy management.World journal of cardiology · 2024Article
- SGLT2i improves kidney senescence by down-regulating the expression of LTBP2 in SAMP8 mice.Journal of cellular and molecular medicine · 2024Article
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Authors and funding
12 authors at 1 institution in 1 country.
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Abstract
Senescent kidney can lead to the maladaptive repairment and predispose age-related kidney diseases. Here, we explore the renal anti-senescence effect of a known kind of drug, sodium-dependent glucose transporters 2 inhibitor (SGLT2i). After 4 months intragastrically administration with dapagliflozin on senescence-accelerated mouse prone 8 (SAMP8) strain mice, the physiologically effects (lowering urine protein, enhancing glomerular blood perfusion, inhibiting expression of senescence-related biomarkers) and structural changes (improving kidney atrophy, alleviating fibrosis, decreasing glomerular mesangial proliferation) indicate the potential value of delaying kidney senescence of SGLT2i. Senescent human proximal tubular epithelial (HK-2) cells induced by H
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