Effect of Glyoxal on Plasma Membrane and Cytosolic Proteins of Erythrocytes DOI Open Access
Michal Kopera,

Malgorzata Adamkiewicz,

Anna Pieniążek

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(9), P. 4328 - 4328

Published: May 2, 2025

Glyoxal (GO) is a reactive dicarbonyl derived endogenously from sugars and other metabolic reactions within cells. Numerous exogenous sources of this compound include tobacco smoking, air pollution, food processing. GO toxic to cells mainly due its high levels reactivity towards proteins, lipids, nucleic acids. We speculate that glyoxal could be involved in erythrocyte protein damage lead cell dysfunction. The osmotic fragility level amino carbonyl groups membrane proteins erythrocytes incubated for 24 h with were identified. amount thiol, amino, was also measured hemolysate after treatment GO. In hemolysate, the glutathione, non-enzymatic antioxidant capacity (NEAC), TBARS, activity enzymes determined. study’s results indicated increases sensitivity, alters glutathione free functional modifies enzymes. Our findings indicate highly human erythrocytes. at concentrations above 5 mM can cause changes disrupt oxidoreductive balance

Language: Английский

Nrf2 Activation in Chronic Kidney Disease: Promises and Pitfalls DOI Creative Commons
Ana Karina Aranda‐Rivera, Alfredo Cruz‐Gregorio, José Pedraza‐Chaverrí

et al.

Antioxidants, Journal Year: 2022, Volume and Issue: 11(6), P. 1112 - 1112

Published: June 3, 2022

The nuclear factor erythroid 2-related 2 (Nrf2) protects the cell against oxidative damage. Nrf2 system comprises a complex network that functions to ensure adequate responses redox perturbations, but also metabolic demands and cellular stresses. It must be kept within physiologic activity range. Oxidative stress alterations in Nrf2-system are central for chronic-kidney-disease (CKD) progression CKD-related morbidity. Activation of CKD is multiple ways related inflammation, kidney fibrosis, mitochondrial effects. In human CKD, both endogenous activation repression exist. state varies with cause disease, comorbidities, stage severity uremic toxin accumulation inflammation. An earlier stage, rapid inflammatory processes associated more robust activation. Advanced stronger repression. moderate kappa B (NF-κB) elevations. relates high NF-κB concentrations, may Kelch-like ECH-associated protein 1 (Keap1)-independent degradation. Furthermore, we review effects pharmacological by bardoxolone methyl, curcumin, resveratrol outline strategies how adapt future Nrf2-targeted therapies requirements patients CKD.

Language: Английский

Citations

42
Efficient selective removal of uremic toxin precursor by olefin-linked covalent organic frameworks for nephropathy treatment DOI Creative Commons

Jinxia Wei,

Rui Li, Penghui Zhang

et al.

Nature Communications, Journal Year: 2023, Volume and Issue: 14(1)

Published: May 16, 2023

Abstract Indoxyl sulfate is a protein-bound uremic toxin synthesized from indole that cannot be efficiently removed by the hemodialysis method and thus becomes key risk factor for progression of chronic kidney disease. Here, we develop non-dialysis treatment strategy to fabricate an ultramicroporous olefin-linked covalent organic framework with high crystallinity in green scalable fashion selectively removing indoxyl precursor (i.e., indole) intestine. Various analyses show resulting material exhibits excellent gastrointestinal fluid stability, adsorption efficiency, good biocompatibility. Notably, it realizes efficient selective removal intestine significantly attenuates serum level vivo. More importantly, efficacy substantially higher than commercial adsorbent AST-120 used clinic. The present study opens up new avenue eliminate further expands vivo applications frameworks.

Language: Английский

Citations

25
Systemic aging fuels heart failure: Molecular mechanisms and therapeutic avenues DOI Creative Commons

Zhuyubing Fang,

Umar Raza,

Jia Song

et al.

ESC Heart Failure, Journal Year: 2024, Volume and Issue: unknown

Published: July 22, 2024

Abstract Systemic aging influences various physiological processes and contributes to structural functional decline in cardiac tissue. These alterations include an increased incidence of left ventricular hypertrophy, a diastolic function, atrial dilation, fibrillation, myocardial fibrosis amyloidosis, elevating susceptibility chronic heart failure (HF) the elderly. Age‐related dysfunction stems from prolonged exposure genomic, epigenetic, oxidative, autophagic, inflammatory regenerative stresses, along with accumulation senescent cells. Concurrently, age‐related changes vascular system, attributed endothelial dysfunction, arterial stiffness, impaired angiogenesis, oxidative stress inflammation, impose additional strain on heart. Dysregulated mechanosignalling nitric oxide signalling play critical roles associated HF. Metabolic drives intricate shifts glucose lipid metabolism, leading insulin resistance, mitochondrial within cardiomyocytes. contribute contractility, ultimately propelling low‐grade conjunction senescence‐associated secretory phenotype, aggravates age by promoting immune cell infiltration into myocardium, fostering This is further exacerbated comorbidities like coronary artery disease (CAD), atherosclerosis, hypertension, obesity, diabetes kidney (CKD). CAD atherosclerosis induce ischaemia adverse remodelling, while hypertension hypertrophy fibrosis. Obesity‐associated inflammation dyslipidaemia create profibrotic environment, whereas diabetes‐related metabolic disturbances impair function. CKD‐related fluid overload, electrolyte imbalances uraemic toxins exacerbate HF through systemic neurohormonal renin‐angiotensin‐aldosterone system (RAAS) activation. Recognizing as modifiable process has opened avenues target both lifestyle interventions therapeutics. Exercise, known for its antioxidant effects, can partly reverse pathological remodelling elderly countering linked HF, such senescence declining cardiomyocyte regeneration. Dietary plant‐based ketogenic diets, caloric restriction macronutrient supplementation are instrumental maintaining energy balance, reducing adiposity addressing micronutrient Therapeutic advancements targeting underway. Key approaches senomorphics senolytics limit senescence, antioxidants stress, anti‐inflammatory drugs interleukin (IL)‐1β inhibitors, rejuvenators nicotinamide riboside, resveratrol sirtuin (SIRT) activators autophagy enhancers metformin sodium‐glucose cotransporter 2 (SGLT2) all which offer potential preserving function alleviating burden.

Language: Английский

Citations

11
Salivary Attenuated Total Reflectance-Fourier Transform Infrared Spectroscopy Combined with Chemometric Analysis: A Potential Point-of-Care Approach for Chronic Kidney Disease Screening DOI Creative Commons

Kamonchanok Tangwanichgapong,

Poramaporn Klanrit,

Patutong Chatchawal

et al.

Photodiagnosis and Photodynamic Therapy, Journal Year: 2025, Volume and Issue: unknown, P. 104502 - 104502

Published: Jan. 1, 2025

Language: Английский

Citations

1
Effect of oral nutritional supplements on inflammation and oxidative stress in hemodialysis patients: a meta-analysis DOI
Tao Shen, Linlin Jiang, Qunjuan Zhang

et al.

International Urology and Nephrology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 24, 2025

Language: Английский

Citations

1
Uremic Toxins and Cardiovascular Risk in Chronic Kidney Disease: What Have We Learned Recently beyond the Past Findings? DOI Creative Commons
Carolla El Chamieh, Sophie Liabeuf,

Ziad Massy

et al.

Toxins, Journal Year: 2022, Volume and Issue: 14(4), P. 280 - 280

Published: April 14, 2022

Patients with chronic kidney disease (CKD) have an elevated prevalence of atheromatous (ATH) and/or non-atheromatous (non-ATH) cardiovascular (CVD) due to array CKD-related risk factors, such as uremic toxins (UTs). Indeed, UTs a major role in the emergence spectrum CVDs, which constitute leading cause death patients end-stage renal disease. The European Uremic Toxin Work Group has identified over 100 UTs, more than 25 are dietary or gut-derived. Even though relationships between and CVDs been described literature, there few reviews on involvement most toxic compounds corresponding physiopathologic mechanisms. Here, we review scientific literature gut-derived greatest toxicity vitro vivo. A better understanding these toxins’ roles among CKD might facilitate development targeted treatments. Hence, (i) ATH non-ATH respective levels (ii) mechanisms that underlie influence CVDs.

Language: Английский

Citations

38
Indole-3-acetic acid exposure leads to cardiovascular inflammation and fibrosis in chronic kidney disease rat model DOI
S.P. Ramya Ranjan Nayak, Seenivasan Boopathi,

Munisamy Chandrasekar

et al.

Food and Chemical Toxicology, Journal Year: 2024, Volume and Issue: 192, P. 114917 - 114917

Published: Aug. 13, 2024

Language: Английский

Citations

7
The AKI-to-CKD Transition: The Role of Uremic Toxins DOI Open Access
Camille André, Sandra Bodeau,

Saı̈d Kamel

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(22), P. 16152 - 16152

Published: Nov. 10, 2023

After acute kidney injury (AKI), renal function continues to deteriorate in some patients. In a pro-inflammatory and profibrotic environment, the proximal tubules are subject maladaptive repair. AKI-to-CKD transition, impaired recovery from AKI reduces tubular glomerular filtration leads chronic disease (CKD). Reduced secretion capacity is characterized by plasma accumulation of biologically active molecules, referred as uremic toxins (UTs). These have role development neurological, cardiovascular, bone, complications CKD. However, UTs might also cause CKD well be consequence. Recent studies shown that these molecules accumulate early contribute establishment this environment kidney. The objective present work was review mechanisms UT toxicity potentially transition each compartment.

Language: Английский

Citations

15
Reno-protective Effects of Empagliflozin in High Fat Diet Induced Obesity-Related Glomerulopathy by Regulation of Gut-Kidney Axis DOI
Lei Lei, Ting Zhu,

Tian-Jiao Cui

et al.

AJP Cell Physiology, Journal Year: 2024, Volume and Issue: 327(4), P. C994 - C1011

Published: Aug. 26, 2024

The increasing prevalence of obesity-related glomerulopathy (ORG) poses a significant threat to public health. Sodium-glucose cotransporter-2 (SGLT2) inhibitors effectively reduce body weight and total fat mass in individuals with obesity halt the progression ORG. However, underlying mechanisms their reno-protective effects ORG remain unclear. We established high-fat diet-induced model using C57BL/6J mice, which were divided into three groups: normal chow diet (NCD group), (HFD) mice treated placebo (ORG HFD empagliflozin (EMPA group). conducted 16S ribosomal RNA gene sequencing feces analyzed metabolites from kidney, feces, liver, serum samples. showed increased urinary albumin creatinine ratio, cholesterol, triglyceride levels, glomerular diameter compared NCD (all P < 0.05). EMPA treatment significantly alleviated these parameters Multitissue metabolomics analysis revealed lipid metabolic reprogramming was altered by treatment. MetOrigin close association between EMPA-related pathways gut microbiota alterations, characterized reduced abundances Firmicutes Desulfovibrio abundance Akkermansia homeostasis especially metabolism, disrupted closely associated contributing improved kidney function morphology regulating metabolism through gut-kidney axis, highlighting novel therapeutic approach for NEW & NOTEWORTHY Our study uncovered that (EMPA) potentially protects renal axis. EMPA's are glycerophospholipid pantothenate/CoA synthesis pathways. modulation appears be pivotal suppressing glycerol 3-phosphate CoA synthesis. insights microbiota-host interactions offer

Language: Английский

Citations

6
Production of Toxins by the Gut Microbiota: The Role of Dietary Protein DOI
Lívia Alvarenga, Julie Ann Kemp,

Beatriz G. Baptista

et al.

Current Nutrition Reports, Journal Year: 2024, Volume and Issue: 13(2), P. 340 - 350

Published: April 8, 2024

Language: Английский

Citations

4