T cells and their products in diabetic kidney disease

Liu, Yue; Lv, Yaodong; Zhang, Tingwei; Huang, Tongtong; Lang, Yating; Sheng, Qinghao; Liu, Yingxiao; Kong, Zhijuan; Gao, Ying; Lu, Shangwei; Yang, Meilin; Luan, Yaqi; Wang, Xining; Lv, Zhimei

doi:10.3389/fimmu.2023.1084448

Cited by 14 publications

(8 citation statements)

References 196 publications

(252 reference statements)

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“…In our study, a high CONUT score was found to be associated with an increased risk of ESRD in patients with diabetic kidney disease, which is the most common complication in these patients. Research has suggested that immune inflammation and nutritional status may be closely related to the progression of renal function in diabetic kidney disease patients ( Zhang et al, 2022 ; Liu et al, 2023 ). Among the components of CONUT score, albumin serves as a cornerstone for nutritional assessment.…”

Section: Discussionmentioning

confidence: 99%

“…Renin-angiotensin system (RAS) inhibitors, sodium-glucose cotransporter-2 inhibitors (SGLT-2is), glucagon-like peptide-1 receptor agonists (GLP-1RAs), and mineralocorticoid receptor antagonist (MRA) have been proven to effectively mitigate the impact of these risk factors on diabetic kidney disease patients ( Yang et al, 2022 ; Filippatos et al, 2023 ; Giglio et al, 2023 ). However, a growing body of research indicates that chronic inflammation, immune dysregulation, and nutritional status also play crucial roles in the progression of diabetic kidney disease ( Yang and Mou, 2017 ; Zhang et al, 2022 ; Liu et al, 2023 ; Zhang et al, 2023 ). As such, early identification and management of these non-traditional risk factors may be critical for optimizing the prognosis of diabetic kidney disease.…”

Section: Introductionmentioning

confidence: 99%

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Controlling nutritional status score is associated with renal progression, cardiovascular events, and all-cause mortality in biopsy-proved diabetic kidney disease

Huo,

He,

Xiong

et al. 2023

Front. Physiol.

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Background: The Controlled Nutritional Status (CONUT) score, calculated from albumin, total cholesterol, and lymphocyte count, is a useful indicator for immune-nutritional assessment and is associated with the prognosis of various diseases. However, its relationship with renal outcomes, cardiovascular disease (CVD), and all-cause mortality in patients with diabetic kidney disease is unclear.Methods: This retrospective single-center study enrolled 336 patients with biopsy-confirmed diabetic kidney disease from August 2009 to December 2018. The outcomes were progression to end-stage renal disease (ESRD), CVD events, and death. Univariate and multivariate Cox regression analyses were performed to estimate the association between confounding factors and outcomes. The Kaplan-Meier curve was used to compare the outcomes of the patients according to the median CONUT score. The area under the curve (AUC) evaluated with time-dependent receiver operating characteristics was used to test discriminative power of COUNT score.Results: During a median follow-up period of 5.1 years. The Kaplan-Meier analysis showed that patients in the high CONUT group (CONUT score > 3) had a significantly higher incidence of ESRD, CVD events, and all-cause mortality than those in the low CONUT group (CONUT score ≤ 3). The multivariate COX regression analysis indicated that, The CONUT score was an independent predictor of ESRD (hazards ration [HR] = 1.129, 95% confidence interval [CI] 1.037-1.228, p = 0.005), CVD events (HR = 1.159, 95% CI 1.057-1.271, p = 0.002), and all-cause mortality (HR = 1.299, 95% CI 1.143-1.478, p < 0.001).Conclusion: The CONUT score is an independent risk factor for ESRD, CVD events, and overall death in patients with diabetic kidney disease.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Controlling nutritional status score is associated with renal progression, cardiovascular events, and all-cause mortality in biopsy-proved diabetic kidney disease

Huo,

He,

Xiong

et al. 2023

Front. Physiol.

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“…Additionally, T cells can directly induce tubular cell apoptosis and contribute to tubulointerstitial fibrosis [ 30 , 31 ]. In diabetic kidney disease, T cells also play a critical role in the pathogenesis of kidney disease [ 32 , 33 ]. T-cell infiltration in the glomerulus is associated with the development of albuminuria and renal fibrosis [ 16 , 34 ].…”

Section: Immunometabolic Alterations In Kidney Diseasementioning

confidence: 99%

The Interplay between Immune and Metabolic Pathways in Kidney Disease

Jiao

2023

Cells

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Kidney disease is a significant health problem worldwide, affecting an estimated 10% of the global population. Kidney disease encompasses a diverse group of disorders that vary in their underlying pathophysiology, clinical presentation, and outcomes. These disorders include acute kidney injury (AKI), chronic kidney disease (CKD), glomerulonephritis, nephrotic syndrome, polycystic kidney disease, diabetic kidney disease, and many others. Despite their distinct etiologies, these disorders share a common feature of immune system dysregulation and metabolic disturbances. The immune system and metabolic pathways are intimately connected and interact to modulate the pathogenesis of kidney diseases. The dysregulation of immune responses in kidney diseases includes a complex interplay between various immune cell types, including resident and infiltrating immune cells, cytokines, chemokines, and complement factors. These immune factors can trigger and perpetuate kidney inflammation, causing renal tissue injury and progressive fibrosis. In addition, metabolic pathways play critical roles in the pathogenesis of kidney diseases, including glucose and lipid metabolism, oxidative stress, mitochondrial dysfunction, and altered nutrient sensing. Dysregulation of these metabolic pathways contributes to the progression of kidney disease by inducing renal tubular injury, apoptosis, and fibrosis. Recent studies have provided insights into the intricate interplay between immune and metabolic pathways in kidney diseases, revealing novel therapeutic targets for the prevention and treatment of kidney diseases. Potential therapeutic strategies include modulating immune responses through targeting key immune factors or inhibiting pro-inflammatory signaling pathways, improving mitochondrial function, and targeting nutrient-sensing pathways, such as mTOR, AMPK, and SIRT1. This review highlights the importance of the interplay between immune and metabolic pathways in kidney diseases and the potential therapeutic implications of targeting these pathways.

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“…[11] Research has demonstrated that the JAK/STAT signaling pathway is closely associated with the pathophysiological processes of kidney diseases. [12] Multiple studies have reported a significant correlation between JAK/STAT signaling and renal fibrosis. [13,14] The reports indicate that CXC chemokine receptor type 4 (CXCR4) activation leads to the activation of JAK2/STAT3 and JAK3/STAT6 signaling in renal cells, subsequently reducing the abundance of glycogen synthase kinase-3beta (GSK3β) mRNA and exacerbating CKD renal fibrosis.…”

Section: Introductionmentioning

confidence: 99%

Hederagenin Improves Adriamycin-induced Nephropathy by Inhibiting the JAK/STAT Signaling Pathway

Zhong,

Jia,

Tan

et al. 2024

Integr Med Nephrol Androl

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Background: Glomerulonephritis, a common kidney disease and major cause of end-stage renal disease, lacks effective treatment options. Hederagenin (HDG) exerts potent anti-inflammatory and protective effects on the kidneys and exhibits promise for the treatment of glomerulonephritis. This study aimed to investigate the therapeutic effects and mechanism of action of hederagenin in the context of adriamycin-induced nephropathy (ADN). Methods: C57BL/6 mice were randomly divided into 5 groups that included the control, model, low-dose HDG (20 mg/kg), high-dose HDG (40 mg/kg), and positive control (10 mg/kg irbesartan) groups. ADN was established in mice by administering a single injection of 10 mg/kg adriamycin. Renal pathology and fibrosis were assessed using haematoxylin and eosin (H & E) and Masson’s trichrome staining, whereas in vitro studies were conducted using cultured mouse podocytes (MPC5). Immunofluorescence staining and western blotting were performed to detect inflammation and the protein levels of signaling pathways. Results: The results revealed that HDG significantly improved adriamycin-induced abnormal serum creatinine, albumin, and urea nitrogen levels. HDG treatment reduced glomerular injury and fibrosis, particularly at high doses. Additionally, HDG effectively reduced adriamycin-induced activation of Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling and renal fibrosis while suppressing CD4+/CD8+ cell ratios in the kidneys and enhancing the immune response. Interestingly, when the JAK/STAT signaling pathway was activated by an agonist, the ameliorative effects of HDG on ADN were inhibited, thus suggesting that JAK/STAT signaling is a key target of HDG. Conclusion: HDG may represent a promising treatment option for glomerulonephritis by inhibiting JAK/STAT-mediated immune-inflammatory responses.

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T cells and their products in diabetic kidney disease

Cited by 14 publications

References 196 publications

Controlling nutritional status score is associated with renal progression, cardiovascular events, and all-cause mortality in biopsy-proved diabetic kidney disease

Controlling nutritional status score is associated with renal progression, cardiovascular events, and all-cause mortality in biopsy-proved diabetic kidney disease

The Interplay between Immune and Metabolic Pathways in Kidney Disease

Hederagenin Improves Adriamycin-induced Nephropathy by Inhibiting the JAK/STAT Signaling Pathway

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