Objective To elucidate the molecular mechanism of sirtuin-3 (SIRT3) in regulating mitochondrial biogenesis in human renal tubular epithelial cells. Methods Cells were stimulated with different concentrations of H₂O₂ and divided into four groups: control (NC), 50 μmol/L H₂O₂, 110 μmol/L H₂O₂ and 150 μmol/L H₂O₂. SIRT3 protein expression was then measured. SIRT3 was knocked down with siRNA, and cells were further assigned to five groups: control (NC), negative-control siRNA (NCsi), SIRT3-siRNA (siSIRT3), NCsi+H₂O₂, and siSIRT3+H₂O₂. After 24 h, cellular adenosine triphosphate (ATP) and mitochondrial superoxide anion (O₂•⁻) levels were determined, together with mitochondrial expression of SIRT3, peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factor 1 (NRF1), mitochondrial transcription factor A (TFAM), superoxide dismutase 2 (SOD2), acetylated-SOD2 and adenosine monophosphate activated protein kinase α1 (AMPKα1). Results The 110 and 150 μmol/L H₂O₂ decreased SIRT3 protein (both P<0.05). ATP and mitochondrial O₂•⁻ did not differ between NC and NCsi groups (both P>0.05). Compared to the NCsi group, the siSIRT3 group exhibited elevated O₂•⁻ level, decreased SIRT3 protein and increased expression levels of SOD2 and acetylated SOD2 protein (all P<0.05). Compared to the NCsi group, the NCsi+H₂O₂ group exhibited decreased cellular ATP levels, elevated mitochondrial O₂•⁻ levels, and reduced protein expression levels of SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 (all P<0.05). Compared with the siSIRT3 group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, SOD2, TFAM, AMPKα1, PGC-1α and NRF1 protein expression levels and a decrease in acetylated SOD2 protein expression levels (all P<0.05). Compared with the NCsi+H₂O₂ group, the siSIRT3+H₂O₂ group showed a decrease in cellular ATP levels, an increase in mitochondrial O₂•⁻ levels, a decrease in SIRT3, AMPKα1, PGC-1α and NRF1, TFAM protein expression levels, and an increase in SOD2 and acetylated SOD2 protein expression levels (all P<0.05). Conclusions SIRT3 promotes mitochondrial biogenesis in tubular epithelial cells via the AMPK/PGC-1α/NRF1/TFAM axis, representing a key mechanism through which SIRT3 ameliorates oxidative stress-induced mitochondrial dysfunction.

AIM: To examine differences in etiology, risk factors, gender, and acute-phase manifestations of retinal artery occlusion(RAO)patients in different age groups, highlighting age-related heterogeneity.

METHODS:This retrospective comparative cohort study enrolled patients with RAO. Patients were divided into <50 y group and ≥50 y group. Etiological classification was based on modified TOAST criteria. Comparisons assessed the prevalence of risk factors, etiological distribution, sex ratio, and, in cases of acute central retinal artery occlusion(CRAO), fundus characteristics and visual outcomes.

RESULTS:This study included a total of 145 RAO patients,which were divided into two groups based on age: <50 y group(15 females and 13 males)with the mean age of 36.64±9.72 y, and ≥50 y group(38 females and 79 males)with the mean age of 63.50±9.54 y. Hypertension(46.4% vs 85.5%)and diabetes(3.6% vs 27.4%)were less prevalent in <50 y group(both P<0.001). The <50 y group was characterized predominantly by stroke of other determined etiology(SOE, 35.7% vs 2.6%, P<0.001), whereas the ≥50 y group was dominated by small artery occlusion(SAO, 35.9%)and large artery atherosclerosis(LAA, 31.6%), the incidence rates were significantly higher in the ≥50 y group than in the <50 y group(both P<0.001). Females were more frequently represented in <50 y group(53.6% vs 32.5%, P=0.039). Multivariable analysis demonstrated that LAA was independently linked to older age and SOE to younger age. Boxcarring occurred exclusively in ≥50 y patients\〖39.5%(17/43)vs 0, P=0.011\〗.

CONCLUSION:The RAO patients<50 y predominantly present with non-atherosclerotic causes and a higher proportion of females, whereas patients≥50 y are mainly affected by atherosclerosis driven etiologies and show signs of reduced vascular compensatory capacity. These findings indicate that age-related differences in RAO should be taken into account when determining etiologic evaluation and management strategies.

Objective To discuss the risk factors of the chronic obstructive nephropathy progression.Methods A retrospective analysis of the patients with chronic obstroctive nephropathy was performed.Multivariate logistic regression was used to identify correlate risk factors of the chronic obstructive nephrupathy progression.All calculation were compu- ted with the aid of SPSS 10.0 software package.Results In the analysis of risk factors of the chronic obstructive ne- phropathy progression,gender(OR=1.963,P=0.018),hypertention(OR=2.228,P=0.039),hyperuricemia (OR=4.204,P=0.000),hypocalcemia(OR=2.612,P=0.031),proteinuric(OR=1.639,P=0.049),hy- poabumia(OR=5.505,P=0.000),SIRS(OR=6.113,P=0.000),anemia(OR=5.257,P=0.000),renal atophy(OR=5.964,P=0.009),contrast medium(OR=6.113,P