Inflammation in glomerular diseases

Frontiers in Immunology, Год журнала: 2025, Номер 16

Опубликована: Март 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

Язык: Английский

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Dead-End protein expression, function, and mutation in cancer: a systematic review

Molecular Biology Reports, Год журнала: 2025, Номер 52(1)

Опубликована: Март 7, 2025

Язык: Английский

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Repurposing Secukinumab and Dapagliflozin as Candidate Therapies to Mitigate the Renal Toxicity of Sunitinib in Rats Through Suppressing IL‐17‐Mediated Pyroptosis and Promoting Autophagy

Journal of Biochemical and Molecular Toxicology, Год журнала: 2025, Номер 39(3)

Опубликована: Март 1, 2025

Sunitinib (SUN) is a chemotherapeutic agent showing renal toxicity that limits its clinical applications. The present research aimed to clarify the potential ameliorative effects of secukinumab (SEC) and dapagliflozin (DAPA) against SUN-induced underpinning molecular mechanisms. For this purpose, adult Wistar albino rats were received SUN (25 mg/kg 3 times/week, po) co-treated with SEC (3 mg/kg/every 2 weeks, subcutaneously) or DAPA (10 mg/kg/day, for 4 weeks compared age-matched control group (CON). Markers kidney functions assessed in serum samples. Kidneys harvested biochemical histological examination. Compared CON group, SUN-treated displayed signs dysfunction along changes ameliorated by DAPA. Both drugs significantly lowered levels IL-17, but exerted more inhibitory effect than Additionally, SUN-subjected showed significant increases expression NLRP3 inflammasome other inflammatory mediators including IL-1β, END-1, MCP-1. This was associated marked decline beclin-1. Co-treatment suppressed NLRP3-induced inflammation while enhanced beclin-1-mediated autophagy. modulatory on beclin-1 superior SEC. Moreover, both similarly attenuated cleaved caspase-3 interstitial fibrosis tissue rats. Collectively, these findings may repurpose as candidate therapies alleviate rescue functionality cancer cases.

Язык: Английский

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Targeting Inflammatory Imbalance in Chronic Kidney Disease: Focus on Anti-Inflammatory and Resolution Mediators

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(7), С. 3072 - 3072

Опубликована: Март 27, 2025

Chronic kidney disease (CKD) is a condition caused by the gradual decline of renal function that approximatively affects 10-12% world population, thus representing public health priority. In CKD patients, chronic and systemic low-grade inflammation observed, it significantly contributes to development progression, especially for patients with advanced disease. It also results in CKD-associated complications increased mortality. The due different factors, such as glomerular filtration rate, immune system activation, reactive oxygen species release, intestinal homeostasis. Therefore, possibility control deserves great attention. this review, we will examine current possible pharmacological approaches counteract inflammatory state CKD, focusing our attention both on pro-inflammatory factors pro-resolving mediators involved state.

Язык: Английский

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A Systematic Review of risk factors for major adverse cardiovascular events in patients with coronary heart disease who underwent percutaneous coronary intervention

Frontiers in Physiology, Год журнала: 2025, Номер 16

Опубликована: Апрель 9, 2025

This study aims to systematically review the risk factors for major adverse cardiovascular events (MACE) in patients with coronary heart disease who have undergone percutaneous intervention (PCI). Systematic and meta-analysis. The Cochrane Library, PubMed, Web of Science, China National Knowledge Infrastructure (CNKI), Wanfang Database, VIP Database Chinese Technical Periodicals (VIP) were screened until December 2024. Case-control studies or cohort on MACE underwent PCI. Data extraction synthesis: literature review, data extraction, quality evaluation conducted by two independent researchers, meta-analysis was performed using RevMan 5.4 software. main outcome that occurred during follow-up period. A total 40 articles included. erevealed dyslipidemia (OR = 1.50; 95% CI [1.19, 1.89], p 0.0007), diabetes mellitus 1.70; [1.43, 2.02], < 0.00001), hypertension 1.62; [1.35, 1.96], 0.0001), history smoking 2.08; [1.51, 2.85], poorer ventricular function 2.39; [2.17-2.64], impaired left ejection fraction (LVEF) 1.86; [1.71-2.03], door balloon (D-to-B) time 0.61; [0.42-0.88]; 0.009), thrombolysis myocardial infarction (TIMI) 1.41; [1.17, 1.70], 0.0004), renal dysfunction 1.82; [1.37, 2.43], multi-vessel artery 0.41; [0.37, 0.46], 0.0001) significantly associated after PCI are dyslipidemia, hypertension, mellitus, history, Killip class > II, LVEF ≤40%, D-to-B >90 min, TIMI flow grade ≤ insufficiency, multivessel disease.

Язык: Английский

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Calycosin and kidney health: a molecular perspective on its protective mechanisms

Pharmacological Reports, Год журнала: 2025, Номер unknown

Опубликована: Апрель 18, 2025

Язык: Английский

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Shen Shuai II Recipe alleviates renal fibrosis in chronic kidney disease by improving of hypoxia and inhibition of TLR4/MyD88/NF-κB/NLRP3 pathway

Renal Failure, Год журнала: 2025, Номер 47(1)

Опубликована: Май 19, 2025

To investigate the anti-fibrotic mechanisms of Shen Shuai II Recipe (SSR) in chronic kidney disease (CKD), focusing on its modulation hypoxia-associated inflammatory pathways and TLR4/MyD88/NF-κB/NLRP3 axis. A 5/6 nephrectomy-induced renal failure (CRF) rat model hypoxia-exposed human tubular epithelial (HK-2) cells were utilized. In vivo, function was assessed via serum creatinine, urea nitrogen, creatinine clearance measurements, alongside histopathological evaluation fibrosis inflammation. vitro, hypoxia-treated HK-2 analyzed for fibrotic markers (fibronectin, collagen I, α-smooth muscle actin) pro-inflammatory cytokines (IL-1β, IL-18). Molecular probed through protein expression analysis HIF-1α TLR4/MyD88/NF-κB pathway, with NLRP3 inflammasome activity evaluated. SSR treatment significantly improved CRF rats, reducing (Scr) nitrogen (BUN) while enhancing clearance. Histopathology revealed preserved architecture attenuated infiltration. hypoxic cells, downregulated suppressed IL-1β IL-18 levels. Mechanistically, reduced expression, inhibited signaling, activation both models. alleviates CKD progression by mitigating hypoxia-driven inflammation blocking pathway.

Язык: Английский

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Semaglutide and adenosine alleviate obesity-induced kidney injury, with observed modulation of the Txnip/NLRP3 pathway

Diabetology & Metabolic Syndrome, Год журнала: 2025, Номер 17(1)

Опубликована: Май 24, 2025

This study was designed to evaluate the effects of Semaglutide and adenosine on kidney protein expression in obese mice induced by a high-fat diet (HFD), identify signaling pathways involved obesity-related glomerulonephropathy (ORG) regulation using proteomics approach. A total 48 were divided into normal-fat (NFD), HFD + semaglutide intervention (HS), (HA) groups. Mouse serum, urine, tissue samples collected markers for blood glucose lipid metabolism, inflammation, oxidative stress (OS), damage protein, urinary protein/creatinine, other relevant factors. The pathological changes observed under light electron microscope. differences proteins kidneys analyzed liquid chromatography-tandem mass spectrometry (LC-MS/MS). with significant selected bioinformatics Western Blot (WB) analyses. can reduce weight mice, improve level OS have positive effect glomerular tubular lesions mice. TXNIP/NLRP3 pathway, which is pathogenesis murine ORG, screened showed that expressions Txn, Txnip, NLRP3 significantly higher than those NFD while levels HS HA substantially lower ameliorate obesity-induced renal injury, potentially through modulation Txnip/NLRP3 pathway.

Язык: Английский

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Targeting the NLRP3 inflammasome for calcium oxalate stones: pathophysiology and emerging pharmacological interventions

Frontiers in Physiology, Год журнала: 2025, Номер 16

Опубликована: Июнь 3, 2025

Kidney stone disease (nephrolithiasis) is a widespread condition affecting millions worldwide, with its prevalence rising due to dietary changes, obesity, and climate-related factors. The formation of kidney stones driven by urinary solute supersaturation, metabolic abnormalities, environmental influences. Calcium oxalate stones, the most common type, result from hypercalciuria, hyperoxaluria, hypocitraturia, often exacerbated high protein intake hormonal imbalances such as hyperparathyroidism. A significant complication their association chronic (CKD). Recurrent contributes renal scarring, obstruction, inflammation, ultimately leading long-term damage. This review explores pivotal role NLRP3 inflammasome in stone-related inflammation. Activated calcium crystals oxidative stress, triggers release pro-inflammatory cytokines (IL-1β IL-18), exacerbating injury fibrosis. Persistent activation linked CKD progression an increased risk end-stage disease. Emerging therapies targeting offer potential strategies mitigate stone-induced inflammation progression. Direct inhibitors MCC950 CP-456773 block activation, reducing inflammatory cytokine release. Indirect approaches, including atorvastatin phenylbutyric acid, address stress mitochondrial dysfunction lower risk. While these treatments show promise preclinical studies, further research needed validate clinical efficacy. Future studies should focus on optimizing NLRP3-targeted therapies, assessing effects prevention Combining antioxidants may enhance protection, providing new avenues for therapeutic intervention.

Язык: Английский

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Mitochondrial Impairment: A Link for Inflammatory Responses Activation in the Cardiorenal Syndrome Type 4

International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(21), С. 15875 - 15875

Опубликована: Ноя. 1, 2023

Cardiorenal syndrome type 4 (CRS 4) occurs when chronic kidney disease (CKD) leads to cardiovascular damage, resulting in high morbidity and mortality rates. Mitochondria, vital organelles responsible for essential cellular functions, can become dysfunctional CKD. This dysfunction trigger inflammatory responses distant organs by releasing Damage-associated molecular patterns (DAMPs). These DAMPs are recognized immune receptors within cells, including Toll-like (TLR) like TLR2, TLR4, TLR9, the nucleotide-binding domain, leucine-rich-containing family pyrin domain-containing-3 (NLRP3) inflammasome, cyclic guanosine monophosphate (cGMP)–adenosine (AMP) synthase (cGAS)–stimulator of interferon genes (cGAS-STING) pathway. Activation these increased expression cytokines chemokines. Excessive chemokine stimulation results recruitment cells into tissues, causing damage. Experimental studies have demonstrated that chemokines upregulated heart during CKD, contributing CRS 4. Conversely, inhibitors been shown reduce inflammation prevent cardiorenal impairment. However, connection between mitochondrial pathways overactivation has not explored. In this review, we delve mechanistic insights discuss how various released CKD activate TLRs, NLRP3, cGAS-STING heart. activation upregulation chemokines, ultimately culminating establishment Furthermore, propose using as potential strategies preventing

Язык: Английский

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