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Vitamin B12 modulates D-galactose-induced renal dysfunction.

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Vitamin B12 supplementation helps manage age-related kidney dysfunction by reducing cellular senescence and oxidative stress. This study shows vitamin B12 alleviates kidney damage markers and improves renal function in aging rats.

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Area of Science:

  • Nephrology
  • Gerontology
  • Biochemistry

Background:

  • Age-related renal impairment is a growing clinical concern.
  • Cellular senescence and oxidative stress are key drivers of age-related chronic kidney disease (CKD).
  • Factors like advanced glycation end products (AGEs) and hyperphosphatemia accelerate senescence and renal dysfunction.

Purpose of the Study:

  • To investigate the protective effects of vitamin B12 on age-related renal dysfunction.
  • To elucidate the underlying mechanisms of vitamin B12 in mitigating kidney aging.
  • To assess vitamin B12's impact on senescence, inflammation, fibrosis, and apoptosis in the aging kidney.

Main Methods:

  • Utilized a D-galactose-induced aging rat model.
  • Administered vitamin B12 to assess its effects on renal function and damage markers.
  • Analyzed signaling pathways related to senescence, phosphate metabolism, inflammation, fibrosis, and apoptosis using qRT-PCR and immunoblotting.

Main Results:

  • Vitamin B12 supplementation attenuated renal dysfunction and alleviated senescence-induced AGEs accumulation and hyperphosphatemia.
  • It reduced inflammation, fibrosis, and apoptosis by modulating RAGE-NFkB, pPERK-GSK3β, and JNK signaling pathways.
  • Vitamin B12 mitigated hyperphosphatemia via the Klotho-FGF23 axis.

Conclusions:

  • Vitamin B12 demonstrates significant potential in managing age-related renal impairment.
  • The findings support vitamin B12 as a therapeutic strategy for preserving kidney function in the elderly.
  • Mechanisms involve regulating senescence, phosphate homeostasis, and inflammatory/fibrotic pathways.