The role of inflammation in diabetic kidney disease

Jung, Su Woong; Moon, Jae‐Young

doi:10.3904/kjim.2021.174

Cited by 38 publications

(73 citation statements)

References 124 publications

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“…Different from previous views that DKD was a metabolic-related disease irrelevant to inflammation, inflammatory mediators, and signaling pathways in the pathogenesis of DKD has recently gained wider acceptance for researchers ( Galkina and Ley, 2006 ; Wada and Makino, 2013 ; Jung and Moon, 2021 ). CircLRP6 participated in HG-induced MC injury by upregulating the expression of Toll-like receptor 4 (TLR4), extensively involved in lipopolysaccharide-induced inflammatory cell injury ( Chen et al, 2019a ; Ciesielska et al, 2021 ).…”

Section: Long Non-coding Rna and Glomerular Mesangial Cell Injurymentioning

confidence: 93%

Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease

Liu

et al. 2022

Front. Cell Dev. Biol.

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Diabetic kidney disease (DKD) is one of the major microvascular complications of diabetes mellitus, with relatively high morbidity and mortality globally but still in short therapeutic options. Over the decades, a large body of data has demonstrated that oxidative stress, inflammatory responses, and hemodynamic disorders might exert critical influence in the initiation and development of DKD, whereas the delicate pathogenesis of DKD remains profoundly elusive. Recently, long non-coding RNAs (lncRNAs), extensively studied in the field of cancer, are attracting increasing attentions on the development of diabetes mellitus and its complications including DKD, diabetic retinopathy, and diabetic cardiomyopathy. In this review, we chiefly focused on abnormal expression and function of lncRNAs in major resident cells (mesangial cell, endothelial cell, podocyte, and tubular epithelial cell) in the kidney, summarized the critical roles of lncRNAs in the pathogenesis of DKD, and elaborated their potential therapeutic significance, in order to advance our knowledge in this field, which might help in future research and clinical treatment for the disease.

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Section: Long Non-coding Rna and Glomerular Mesangial Cell Injurymentioning

confidence: 93%

Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease

Liu

et al. 2022

Front. Cell Dev. Biol.

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“…In recent years, the role of chronic inflammation in the progression of DKD has been the subject of increasing research (10). Neutrophils are the largest number of white blood cells in the peripheral blood and play an extremely critical role in the immune response.…”

Section: Original Articlementioning

confidence: 99%

Midkine promotes kidney injury in diabetic kidney disease by increasing neutrophil extracellular traps formation

Liu¹,

Ren²,

You-song³

et al. 2022

Ann Transl Med

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Background: We sought to investigate the role of midkine (MK) on neutrophil extracellular trap formation (NETosis) and diabetic kidney disease (DKD) progression. Methods: The expression of MK and NETosis in the renal tissue of DKD patients was examined by immunohistochemistry and immunofluorescence, respectively. Neutrophils extracted from mouse bone marrow by gradient centrifugation were treated with MK for this in-vitro study. A mouse diabetes model was induced by a high-fat diet combined with an intraperitoneal injection of streptozocin (STZ). Antisense oligodeoxynucleotide (ODN) for MK inhibition was administered via tail vein injection. Results: We found that the expression of MK was increased in the kidney tissue of DKD patients. Additionally, a greater number of neutrophils were primed toward NETosis in the kidney tissue of DKD patients, which was manifested by the increased expression of NETosis biomarkers citrullinated histone H3 (H3Cit) and myeloperoxidase (MPO). In vitro, MK treatment concentration-dependently increased neutrophil proliferation (cell counting kit-8). Further, western blot and enzyme-linked immunosorbent assays showed that MK (100 ng/mL) significantly promoted NETosis and the expression of inflammatory factors interleukin (IL)-1 and IL-6 secretion in high-glucose treated neutrophils. In the mouse diabetes model, MK promoted the pathological damage and fibrosis of kidney tissue, as demonstrated by the reversion of the pathological damage and fibrosis by the MK antisense ODN [diabetes mellitus (DM) + MK -ODN] treatment. Additionally, the inhibition of MK reduced the formation of NETs. Conclusions: MK promotes DKD progression by increasing NETosis.

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“…Moreover, CKD itself is one of the strongest risk factors for cardiovascular events. These risk factors lead to endothelial cell injury, which eventually results in end organ damage [ 4 ]. Recent studies have examined the mechanism of the crosstalk between the kidney and other organs [ 5 , 6 ].…”

Section: Introductionmentioning

confidence: 99%

Emotional and cognitive changes in chronic kidney disease

Kim

Gil

2022

Korean J Intern Med

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Chronic kidney disease (CKD) leads to cognitive impairment and emotional changes. However, the precise mechanism underlying the crosstalk between the kidneys and the nervous system is not fully understood. Inflammation and cerebrovascular disease can influence the development of depression in CKD. CKD is one of the strongest risk factors for cognitive impairment. Moreover, cognitive impairment occurs in CKD as patients experience the dysregulation of several brain functional domains due to damage caused to multiple cortical regions and to subcortical modulatory neurons. The differences in structural brain changes between CKD and non-CKD dementia may be attributable to the different mechanisms that occur in CKD. The kidney and brain have similar anatomical vascular systems, which may be susceptible to traditional risk factors. Vascular factors are assumed to be involved in the development of cognitive impairment in patients with CKD. Vascular injury induces white matter lesions, silent infarction, and microbleeds. Uremic toxins may also be directly related to cognitive impairment in CKD. Many uremic toxins, such as indoxyl sulfate, are likely to have an impact on the central nervous system. Further studies are required to identify therapeutic targets to prevent changes in the brain in patients with CKD.

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The role of inflammation in diabetic kidney disease

Cited by 38 publications

References 124 publications

Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease

Long Non-Coding RNAs in the Pathogenesis of Diabetic Kidney Disease

Midkine promotes kidney injury in diabetic kidney disease by increasing neutrophil extracellular traps formation

Emotional and cognitive changes in chronic kidney disease

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