Vitamin B12 modulates D-galactose-induced renal dysfunction.

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.