Characterization and Role of Glucagon-Like Peptide 1 Receptor in the Lacrimal Gland: Novel Insights into Diabetic Dry Eye Pathogenesis DOI
Yan Sun, Yue Zhang, Fan Shi

et al.

American Journal Of Pathology, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 1, 2024

Language: Английский

The role of M1/M2 macrophage polarization in the pathogenesis of obesity-related kidney disease and related pathologies DOI Creative Commons

Periklis Dousdampanis,

Ιωάννα Αγγελετοπούλου, Αthanasia Mouzaki

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 10, 2025

Obesity is a rapidly growing health problem worldwide, affecting both adults and children increasing the risk of chronic diseases such as type 2 diabetes, hypertension cardiovascular disease (CVD). In addition, obesity closely linked to kidney (CKD) by either exacerbating diabetic complications or directly causing damage. Obesity-related CKD characterized proteinuria, lipid accumulation, fibrosis glomerulosclerosis, which can gradually impair function. Among immune cells innate adaptive response involved in pathogenesis obesity-related diseases, macrophages play crucial role inflammation associated with CKD. obese individuals, enter pro-inflammatory state known M1 polarization, contributes inflammation. This polarization promotes tissue damage, fibrosis, leading progressive loss macrophage-induced oxidative stress key feature it also cell damage Macrophages contribute insulin resistance diabetes releasing inflammatory molecules that glucose metabolism, complicating management patients. Hypertension atherosclerosis, are often obesity, progression via pathways. influence blood pressure regulation vascular inflammation, particularly renin-angiotensin system. accumulate arterial plaques, plaque instability, may increase CVD review focuses on involvement highlights their critical link between other pathologies. Targeting macrophage ensuing could be an effective therapeutic strategy for related improve outcomes patients disease.

Language: Английский

Citations

2

Proliferation of renal macrophage via MR/CSF1 pathway induced with aldosterone and inhibited by esaxerenone DOI
Ziqian Liu,

R. Lv,

Haixia Guo

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 149, P. 114208 - 114208

Published: Feb. 8, 2025

Language: Английский

Citations

1

Protective effects and possible mechanisms of mesenchymal stem cells and mesenchymal stem cell-derived extracellular vesicles against kidney fibrosis in animal models: a systematic review and meta-analysis DOI Creative Commons
Yang Lv, Hua Zhang, Xiaomei Lü

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 15

Published: Jan. 3, 2025

The risk of kidney fibrosis is significantly elevated in individuals with diabetes, chronic nephritis, trauma, and other underlying conditions. Concurrently, human umbilical cord blood-derived mesenchymal stem cells (hUCB-MSCs) their extracellular vesicles (MSC-Exos) have gained prominence regenerative medicine. In light these observations, we are undertaking a meta-analysis to elucidate the influence hUCB-MSCs MSC-Exos on fibrosis. To identify eligible trials, conducted comprehensive search CNKI, PubMed, Web Science Wanfang databases from inception 24 October 2022. Furthermore, methodological quality included studies was evaluated using Systematic Review Center for Laboratory Animal Experimentation (SYRCLE) risk-of-bias tool. Besides, weighted standard mean difference (SMD) 95% confidence interval (CI) calculated Manager 5.4 software. Stata (12.0) software employed assess impact factors outcome heterogeneity publication bias study. A total 645 related research were retrieved, which 14 that involved 219 experimental animals comparison control treatment, treatment Human UCB MSC observed enhance renal function animal models This evidenced by reduction serum creatinine (Scr) levels (p < 0.00001) blood urea nitrogen (BUN) 0.00001), as well CD68+ macrophages TdT-mediated dUTP Nick-End labeling (TUNEL)+ tubular cells(p α-SMA = 0.0009) TGF-β1 0.00001). P 0.05 deemed indicate statistically significant difference. Alpha-smooth muscle actin (α-SMA) specific protein normally expressed myofibroblasts. term "CD68+ macrophages" refers express CD68 cell surface. Both myofibroblasts been linked development this study, quantity means gauging extent Additionally, transforming growth factor beta 1 (TGF-β1) cytokine implicated pathogenesis TUNEL-positive represent undergoing apoptosis. It hypothesized may result apoptosis delay fibrosis, due inhibition transformation into (MMT) disruption fibrogenic niche. principal findings preclinical systematic review hUCB substantial protective against Kidney transfer remains final option traditional treatment. lack donors high cost make it challenging many patients access appropriate Although study still suffers three shortcomings: sample size, consistency translational challenges, demonstrated reduce inhibit fibrotic progression. offer promising alternative lower price accessibility. Nevertheless, further high-quality required future address limitations identified review. Identifier INPLASY2022100104.

Language: Английский

Citations

0

DYNAMICS OF THE CONCENTRATION OF PROFIBROGENIC BIOMARKERS IN BLOOD AND URINE IN PATIENTS WITH ACUTE UPPER URINARY TRACT OBSTRUCTION DOI Creative Commons
I. M. Dovbysh,

Г. В. Бачурин

Bulletin of Problems Biology and Medicine, Journal Year: 2025, Volume and Issue: 1(1), P. 194 - 194

Published: Jan. 1, 2025

Language: Английский

Citations

0

Tissue-resident macrophages and renal diseases: landscapes and treatment directions DOI Creative Commons
Zhuojian Qu,

Jinjin Chu,

Shuyu Jin

et al.

Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 16

Published: March 31, 2025

Tissue-resident macrophage (TRM) is a specialized subset of that resides within specific tissues and organs. TRMs play crucial roles in resisting pathogen invasion, maintaining the homeostasis immune microenvironment, promoting tissue repair regeneration. The development function exhibit significant heterogeneity across different tissues. Kidney (KTRMs) originate from both embryonic yolk sac erythro-myeloid progenitors fetal liver, demonstrating capacity for self-renewal independent bone marrow hematopoiesis. KTRMs are not only essential maintenance renal monitoring microvascular environment, but contribute to injury due inflammation, fibrosis dysfunction kidneys. In this review, we summarize currently available studies on regulatory role processes repair. altering effects underlying mechanisms regulating local cells diseases reviewed, primarily including lupus nephritis, diabetic nephropathy, fibrosis, carcinoma. Understanding plasticity functions may offer new insights into pathogenesis exploration therapeutic strategies kidney diseases.

Language: Английский

Citations

0

Macrophage Depletion Alleviates Immunosenescence in Diabetic Kidney by Modulating GDF-15 and Klotho DOI Open Access
Asma S. Alonazi,

Rana M. Aloraini,

Lama M. Albulayhi

et al.

International Journal of Molecular Sciences, Journal Year: 2025, Volume and Issue: 26(9), P. 3990 - 3990

Published: April 23, 2025

Cellular senescence is a hallmark of aging and contributes to age-related diseases, including diabetic nephropathy (DN). Additionally, macrophage-mediated inflammation has been linked with DKD. Therefore, we investigated the effect macrophage depletion on kidney cell in DN, focusing relationship between GDF-15 Klotho signaling pathways. Wistar albino rats (n = 24) were divided into four groups: healthy control, liposomal clodronate (LC)-treated healthy, diabetic, LC-treated groups. Rats groups intravenously administered LC once week for 4 weeks. Rat models type 2 diabetes successfully established via administration streptozotocin high-fat diet, as evidenced by increased blood glucose levels, weight body (KW/BW) ratio, serum albumin, creatinine, urea damage, oxidative stress. However, LC-mediated reduced KW/BW improved parameters, decreased inflammatory markers (IL-6 TNF-α), ameliorated treatment promoted polarization towards anti-inflammatory phenotype, downregulated expression, upregulated damage. In conclusion, combats modulating GDF-15, indicating their potential novel targets DN treatment.

Language: Английский

Citations

0

Macrophage-Induced Pro-Fibrotic Gene Expression in Tubular Cells after Ischemia/Reperfusion Is Paralleled but Not Directly Mediated by C5a/C5aR1 Signaling DOI Creative Commons
Erik Bleich, Eva Vonbrunn, Maike Büttner‐Herold

et al.

Life, Journal Year: 2024, Volume and Issue: 14(8), P. 1031 - 1031

Published: Aug. 19, 2024

Ischemia/reperfusion (I/R) is inevitable during kidney transplantation and causes acute injury (AKI), which affects immediate outcome leads to chronic changes such as fibrotic remodeling of the graft. We investigated pro-fibrotic signaling after I/R, focusing on complement component receptor C5a/C5aR1 macrophage/tubule crosstalk. Male Dark Agouti rats were subjected I/R their kidneys harvested 10 min, 6 h, 24 3 days, 5 days 8 weeks reperfusion. The development renal fibrosis was assessed by detection Vimentin (VIM), α-smooth muscle actin (α-SMA) collagen immunohistochemistry Sirius Red staining, respectively. characterization activity C5aR1+ cells performed multiplex mRNA analysis, ELISA, immunofluorescence flow cytometry in situ hybridization animal models cell culture analyses. In experiments, we focused crosstalk co-culture experiments mimicked vivo conditions hypoxia/reoxygenation supplementation with C5a. Already 6-24 h induction rat model, C5a concentration plasma significantly increased compared control. matrix components VIM α-SMA peaked day declined weeks, when an increase detected using Red. contrast early I/R-induced activation,

Language: Английский

Citations

0

Characterization and Role of Glucagon-Like Peptide 1 Receptor in the Lacrimal Gland: Novel Insights into Diabetic Dry Eye Pathogenesis DOI
Yan Sun, Yue Zhang, Fan Shi

et al.

American Journal Of Pathology, Journal Year: 2024, Volume and Issue: unknown

Published: Dec. 1, 2024

Language: Английский

Citations

0