BMC Public Health, Journal Year: 2024, Volume and Issue: 24(1)
Published: Aug. 15, 2024
Parkinson's disease (PD) is a neurodegenerative influenced by various clinical factors. The potential relationship between renal function and the risk of PD remains poorly understood. This study aims to explore association kidney developing PD.
Language: Английский
Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)
Published: Feb. 28, 2025
The purpose of the study was to investigate renal oxidative stress (OS) and its relationship with disease severity in patients chronic kidney (CKD) using positron emission tomography coupled magnetic resonance imaging (PET/MRI), employing 64Cu-diacetyl-bis(N4-methylthiosemicarbazonate) (64Cu-ATSM) as PET tracer for OS imaging. Thirty CKD (66.4 ± 8.2 y.o.) seven healthy controls (HC) subjects (58.3 3.8 underwent 64Cu-ATSM PET/MRI. Participants were categorized into three groups based on their estimated glomerular filtration rate (eGFR): HC, mild (stages 2-3a), advanced 3b-5). All 30-min dynamic PET/MRI starting injection evaluate blood flow (RBF) levels. RBF (mL/min/100 g) images calculated from first 3 min data, standardized uptake value (SUV) obtained delayed frames 15-30 after injection. SUV corrected RBF-adjusted individual estimate levels kidneys following equation: adjusted index (aOSi) = (SUV/RBF)x100. Significant correlation observed between eGFR (r 0.81, P < 0.001). is significantly lower than that HC (P 0.001) 0.004). did not differ among 0.171). SUVs correlate creatinine or CKD. However, these values 0.33, 0.049) all subjects, whereas showed no significant correlation. Following correction, aOSi demonstrated correlations 0.75, 0.001), (r= -0.65, stages 0.57, subjects. This preliminary has revealed may provide a reasonably noninvasively. Increased correlated levels, suggesting increases dysfunction.
Language: Английский
Citations
0
International Urology and Nephrology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 28, 2025
Language: Английский
Citations
0
Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16
Published: March 4, 2025
The structural and functional integrity of glomerular cells is critical for maintaining normal kidney function. Glomerular diseases, which involve chronic histological damage to the kidney, are related injury such as endothelial cells, mesangial (MCs), podocytes. When faced with pathogenic conditions, these release pro-inflammatory cytokines chemokines, inflammatory factors, adhesion factors. These substances interact through specific pathways, resulting in structure function glomeruli, ultimately causing disease. Although role inflammation diseases well known, molecular pathways that result remain largely unclear. For a long time, it has been believed only immune can secrete Therefore, targeted therapies against were considered first choice treating However, emerging research indicates non-immune MCs, podocytes also play renal by releasing Similarly, should be considered. This review aims uncover inflammation, time summarized glomerulus participate secreting providing valuable references future strategies prevent treat diseases. More importantly, we emphasized cell therapy, may key direction treatment
Language: Английский
Citations
0
Biomolecules, Journal Year: 2025, Volume and Issue: 15(4), P. 556 - 556
Published: April 9, 2025
Renal fibrosis is a critical pathological feature of various chronic kidney diseases, with hypoxia being recognized as an important factor in inducing fibrosis. Yaks have long inhabited high-altitude hypoxic environments and do not exhibit fibrotic damage under hypoxia. However, the underlying protective mechanisms remain unclear. This study compared renal tissue structure collagen volume between low-altitude cattle yaks, revealing that yaks possess significantly higher number tubules than cattle, though showed no significant difference. Under treatment, we observed induced but did show effect suggesting adaptation may anti-fibrotic effect. Further investigation demonstrated upregulation P-AMPK/AMPK, Parkin, PINK1, LC3Ⅱ/Ⅰ, BECN1, alongside downregulation P-mTOR/mTOR yak kidneys. Additionally, hypoxia-induced tubular epithelial cells (RTECs) increased expression mitophagy-related proteins, mitochondrial membrane depolarization, lysosomes, indicating induces mitophagy. By regulating mitophagy pathway through drugs, found hypoxia, activation upregulated E-cadherin protein while downregulating Vimentin, α-SMA, Collagen I, Fibronectin. Simultaneously, there was increase SLC7A11, GPX4, GSH levels, decrease ROS, MDA, Fe2⁺ accumulation. Inhibition produced opposite effects on cellular markers. studies identified ferroptosis key mechanism promoting Moreover, models, reduced accumulation Fe2⁺, thereby alleviating ferroptosis-induced These findings suggest protects from by activating to inhibit pathway.
Language: Английский
Citations
0
Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown
Published: April 14, 2025
Language: Английский
Citations
0
Mitochondrion, Journal Year: 2025, Volume and Issue: unknown, P. 102042 - 102042
Published: April 1, 2025
Language: Английский
Citations
0
Environmental Toxicology, Journal Year: 2024, Volume and Issue: 39(6), P. 3679 - 3693
Published: March 21, 2024
Abstract Environmental arsenic exposure is one of the major global public health problems. Studies have shown that can cause renal fibrosis, but underlying mechanism still unclear. Integrating in vivo and vitro models, this study investigated potential molecular pathways for arsenic‐induced fibrosis. In study, SD rats were treated with 0, 5, 25, 50, 100 mg/L NaAsO 2 8 weeks via drinking water, HK2 cells different doses 48 h. The results showed content rats' kidneys increased as dose increased. Body weight decreased kidney coefficient at mg/L. As a response to elevated dose, inflammatory cell infiltration, tubular injury, glomerular atrophy, tubulointerstitial hemorrhage, fibrosis became more obvious indicated by HE Masson staining. transcriptome profiles further supported protein–protein interactions involved ‐induced results, together experiments, revealed disturbed mitochondrial dynamics, promoted mitophagy, activated inflammation TGF‐β1/SMAD signaling pathway, finally resulted summary, contributed regulating dynamics NLRP3‐TGF‐β1/SMAD axis. This presented an adverse outcome pathway development due through water.
Language: Английский
Citations
3
Biomedicine & Pharmacotherapy, Journal Year: 2024, Volume and Issue: 171, P. 116144 - 116144
Published: Jan. 9, 2024
Mitochondrial dysfunction is one of the key mechanisms for developing chronic kidney disease (CKD). Hyperoxaluria and nephrolithiasis are also associated with mitochondrial dysfunction. Increasing evidence has shown that caffeine, main bioactive compound in coffee, exerts both anti-fibrotic anti-lithogenic properties but unclear mechanisms. Herein, we address protective effect caffeine against during oxalate-induced epithelial-mesenchymal transition (EMT) renal cells. Analyses revealed oxalate successfully induced EMT MDCK cells as evidenced by increased expression several EMT-related genes (i.e., Snai1, Fn1 Acta2). Oxalate suppressed cellular metabolic activity intracellular ATP level, reactive oxygen species (ROS). Additionally, reduced abundance active mitochondria fragmentation (fission). Furthermore, decreased biogenesis content sirtuin-1 (SIRT1), peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α), cytochrome c oxidase subunit 4 (COX4), total proteins. Nonetheless, these deteriorations their were hampered caffeine. Knockdown Snai1 gene small interfering RNA (siRNA) completely abolished effects on suppression activity, mitochondria, indicating cell mediated through gene. These data, at least part, unveil mechanism preserving function.
Language: Английский
Citations
2
Mitochondrion, Journal Year: 2024, Volume and Issue: 76, P. 101869 - 101869
Published: March 11, 2024
Language: Английский
Citations
2
Frontiers in Endocrinology, Journal Year: 2024, Volume and Issue: 15
Published: July 23, 2024
Diabetic nephropathy (DN) is a microvascular complication of diabetes mellitus. The progressive damage to glomeruli, tubules, and interstitium in the kidneys can lead development chronic kidney disease (CKD) end-stage renal (ESRD). Most energy we need comes from mitochondria. Mitochondria are best known as sites for production respiratory ATP essential eukaryotic life. pathogenesis DN involves variety factors, such altered haemodynamics, oxidative stress, inflammation, studies animal models suggest that mitochondrial dysfunction plays an important role DN. Traditional Chinese medicine (TCM) has history more than 2,500 years rich experience remarkable efficacy treatment Recent have found TCM may great potential regulating This review will elucidate main causes relationship with DN, explore depth mechanisms protect by improving dysfunction. Current pharmacological treatments patients do not prevent inevitable progression ESRD. With herbs, expected be most promising candidate continue learn about incorporate current advances extraction techniques.
Language: Английский
Citations
2