Journal of Colloid and Interface Science, Journal Year: 2024, Volume and Issue: 678, P. 174 - 187
Published: Sept. 1, 2024
Language: Английский
Cell Communication and Signaling, Journal Year: 2025, Volume and Issue: 23(1)
Published: Jan. 28, 2025
Oxidative stress-associated proximal tubular cells (PTCs) damage is an important pathogenesis of hypertensive renal injury. We previously reported the protective effect VEGFR3 in salt-sensitive hypertension. However, specific mechanism underlying role kidney during overactivation renin-angiotensin-aldosterone system remains unclear. In present study, nephropathy was established by angiotensin II (Ang II). found that highly increased PTCs Ang II-infused mice. Activation mitigated dysfunction, pathological damage, and oxidative stress II-induced Moreover, we restored mitophagy deficiency induced both vivo vitro to alleviate injury PTCs. Furthermore, experiment demonstrated improved abnormal enhancing PARKIN mitochondrial translocation. LC-MS/MS Co-IP assays identified HSPA1L as interacted protein VEGFR3, which promoted translocation PARKIN. Mechanistically, disorder domain bound HSPA1L, crotonylation modification at K130 required for regulation context Finally, on were attenuated transfection (HSPA1L-K130R) mutant plasmid vitro. These findings indicated alleviated promoting PARKIN-dependent pathway via regulating site PTCs, provided a mechanistic basis therapeutic target
Language: Английский
Citations
2
ACS Omega, Journal Year: 2025, Volume and Issue: 10(6), P. 5148 - 5171
Published: Feb. 3, 2025
Alzheimer's disease (AD) is an aging-related irreversible neurodegenerative affecting mostly the elderly population. The main pathological features of AD are extracellular Aβ plaques generated by APP cleavage through amyloidogenic pathway, intracellular neurofibrillary tangles (NFT) resulting from hyperphosphorylated tau proteins, and cholinergic neurodegeneration. However, actual causes unknown, but several studies suggest hereditary mutations in PSEN1 -2, APOE4, APP, TAU genes major perpetrators. In order to understand etiology pathogenesis AD, various hypotheses proposed. These include following hypotheses: amyloid accumulation, tauopathy, inflammation, oxidative stress, mitochondrial dysfunction, glutamate/excitotoxicity, deficiency, gut dysbiosis. Currently approved therapeutic interventions donepezil, galantamine, rivastigmine, which cholinesterase inhibitors (ChEIs), memantine, N-methyl-d-aspartate (NMDA) antagonist. treatment strategies focus on only symptomatic management attenuating symptoms not regeneration neurons or clearance Tau. This review focuses pathophysiology, novel targets, disease-altering treatments such as α-secretase modulators, active immunotherapy, passive natural antioxidant products, nanomaterials, antiamyloid therapy, aggregation inhibitors, transplantation fecal microbiota stem cells, microtubule stabilizers that clinical trials still under investigation.
Language: Английский
Citations
1
Clinics in Liver Disease, Journal Year: 2024, Volume and Issue: 28(4), P. 633 - 646
Published: July 23, 2024
Language: Английский
Citations
5
Animals, Journal Year: 2024, Volume and Issue: 14(9), P. 1359 - 1359
Published: April 30, 2024
This study investigated the efficacy of a composite probiotics composed
Language: Английский
Citations
4
Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)
Published: Sept. 26, 2024
Language: Английский
Citations
4
Hepatology Communications, Journal Year: 2024, Volume and Issue: 8(11)
Published: Oct. 24, 2024
Excessive alcohol consumption is a leading cause of alcohol-associated liver disease (ALD), significant global health concern with limited therapeutic options. Understanding the key factors contributing to ALD pathogenesis crucial for identifying potential targets. Central intricate interplay between metabolism and cellular processes, particularly involving mitochondria. Mitochondria are essential organelles in liver, critical energy production metabolic functions. However, they vulnerable alcohol-induced damage due their involvement metabolism. Alcohol disrupts mitochondrial function, impairing ATP triggering oxidative stress, which leads inflammation. Mitochondrial quality control mechanisms, including biogenesis, dynamics, mitophagy, maintaining optimal function. Chronic checkpoints, dysfunction that impairs fatty acid oxidation contributes hepatic steatosis ALD. Moreover, promotes accumulation damaged mitochondria release proinflammatory components, exacerbating Preserving presents promising approach mitigate progression. In this review, we provide comprehensive overview effects on function highlighting role pathogenesis. these mechanisms may pave way development novel interventions
Language: Английский
Citations
4
Environment International, Journal Year: 2024, Volume and Issue: 193, P. 109109 - 109109
Published: Nov. 1, 2024
Micro/Nano plastics (MNPs) pollutants are widespread in the environment, raising significant concerns about their biosafety. Emerging studies indicate that urinary system is a primary accumulation site for MNPs, leading to severe tissue and functional damage. This review aims summarize recent research on potential hazards MNPs may pose system, highlighting mechanisms of toxicity current state knowledge. Studies have shown enter human body through drinking water, food chain, inhalation, skin contact. They penetrate bloodstream via digestive, respiratory, systems, subsequently dispersing various organs, including system. The might induce cellular oxidative stress, inflammation, apoptosis, autophagy, "intestine-kidney axis", other possible toxic mechanisms. These processes could disrupt kidney metabolic functions promote fibrosis, thereby potentially increasing risk diseases. Despite ongoing research, understanding MNPs' impact remains limited. Therefore, this provides comprehensive overview highlights key challenges, outlines future directions. It offers theoretical basis development effective protective measures policies.
Language: Английский
Citations
4
Antioxidants, Journal Year: 2024, Volume and Issue: 13(11), P. 1386 - 1386
Published: Nov. 14, 2024
Background: The gut microbiota constitutes a complex microorganism community that harbors bacteria, viruses, fungi, protozoa, and archaea. human bacterial has been extensively proven to participate in metabolism, immunity, nutrient absorption. Its imbalance, namely “dysbiosis”, linked disordered metabolism. Metabolic dysfunction-associated steatotic liver disease (MASLD) is one of the features deranged metabolism leading cause cirrhosis hepatocellular carcinoma. Thus, there pathophysiological link between dysbiosis MASLD. Aims Methods: We aimed review literature data on composition its MASLD describe concept “gut–liver axis”. Moreover, we reviewed approaches for modulation treatment. Results: There consolidated evidence particular associated with stages. model explaining relationship bidirectional organization, physiopathology Oxidative stress keystones pathophysiology fibrosis generation. promising efficacy pre- probiotics reversing patients, therapeutic effects. Few yet encouraging fecal transplantation (FMT) are available literature. Conclusions: characteristic key target reversal treatment via diet, pre/probiotics, FMT remains treatment, prevention, reversal.
Language: Английский
Citations
4
Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)
Published: Feb. 6, 2025
This study aimed to determine whether remnant cholesterol (RC) and its variability can predict the onset of metabolic dysfunction-associated steatotic liver disease (MASLD) independently low-density lipoprotein (LDL-C) levels. A longitudinal cohort involving 43,065 participants who underwent at least two physical examinations was conducted. used Cox proportional hazards models assess relationships among RC quartile levels (Q1–Q4), visit-to-visit variability, risk MASLD. quantified using several metrics: standard deviation (SD), logSD, average real (ARV), logARV, mean absolute (MAD), logMAD. Concurrently, this utilized a combined analysis LDL-C groups independent MASLD associated with RC. During 3.19 years (SD 2.06 years), 8374 patients (19.45%) developed Compared Q1, Q4 significantly greater (hazard ratio [HR] 1.309, 95% confidence interval [CI] 1.220–1.403, P < 0.001). The fully adjusted model revealed that HRs SD, ARV, MAD logMAD were 1.400 (95% CI 1.305–1.502), 1.278 1.188–1.374), 1.152 1.079–1.229), 1.183 1.140–1.227), 1.578 1.433–1.737) 1.263 1.175–1.358), respectively. In both subgroups (≥ 3.4 mmol/L mmol/L), high baseline elevated (HR 1.208, 1.148–1.270, 0.001; HR 1.246, 1.129–1.374, in healthy individuals, irrespective level. during periods provides predictive marker for identifying individuals heightened
Language: Английский
Citations
0
American Journal Of Pathology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 1, 2025
Language: Английский
Citations
0