Complement C5 activation promotes type 2 diabetic kidney disease via activating STAT3 pathway and disrupting the gut‐kidney axis

Li, Ling; Wei, Tiantian; Liu, Shuyun; Wang, Chengshi; Zhao, Meng; Feng, Yanhuan; Ma, Liang; Liu, Yanrong; Fu, Ping; Liu, Jingping

doi:10.1111/jcmm.16157

Cited by 41 publications

(34 citation statements)

References 60 publications

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“…The upregulation of the complement system plays an important role in the development of T1DM and T2DM, as well as in the pathogenesis of the complications of DM [60]. It was documented that the complement system plays a significant role in the development of diabetic kidney disease [61][62][63], retinopathy [64], and periodontal destruction in patients with DM [65]. Interestingly, the mechanism by which the complement system promotes the development of diabetic kidney disease is the activating of the signal transducer and activator of transcription 3 (STAT3) pathway [63].…”

Section: Complement Systemmentioning

confidence: 99%

Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes

Jakubiak

Pawlas

Cieślar

et al. 2021

IJERPH

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Diabetes mellitus (DM) is a strong risk factor for the development of cardiovascular diseases such as coronary heart disease, cerebrovascular disease, and peripheral arterial disease (PAD). In the population of people living with DM, PAD is characterised by multi-level atherosclerotic lesions as well as greater involvement of the arteries below the knee. DM is also a factor that significantly increases the risk of lower limb amputation. Percutaneous balloon angioplasty with or without stent implantation is an important method of the treatment for atherosclerotic cardiovascular diseases, but restenosis is a factor limiting its long-term effectiveness. The pathogenesis of atherosclerosis in the course of DM differs slightly from that in the general population. In the population of people living with DM, more attention is drawn to such factors as inflammation, endothelial dysfunction, platelet dysfunction, blood rheological properties, hypercoagulability, and additional factors stimulating vascular smooth muscle cell proliferation. DM is a risk factor for restenosis. The purpose of this paper is to provide a review of the literature and to present the most important information on the current state of knowledge on mechanisms and the clinical significance of restenosis and in-stent restenosis in patients with DM, especially in association with the endovascular treatment of PAD. The role of such processes as inflammation, neointimal hyperplasia and neoatherosclerosis, allergy, resistance to antimitotic drugs used for coating stents and balloons, genetic factors, and technical and mechanical factors are discussed. The information on restenosis collected in this publication may be helpful in planning further research in this field, which may contribute to the formulation of more and more precise recommendations for the clinical practice.

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Section: Complement Systemmentioning

confidence: 99%

Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes

Jakubiak

Pawlas

Cieślar

et al. 2021

IJERPH

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“…C5 can promote DKD by activating the STAT3 pathway and inducing inflammation in the kidneys, but SCFAs can partially offset its injurious effects. 53 A gut microbiome‐immune axis exists in the human body. Gut microbiota‐derived metabolites can pass through the intestinal epithelium and accumulate in the circulatory system.…”

Section: Mechanisms Behind the Effects Of Gut Microbiota On Dkdmentioning

confidence: 99%

Gut microbiota, key to unlocking the door of diabetic kidney disease

Wang

Zheng

et al. 2021

Nephrology

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“…miRNA-hub gene regulatory network and TF-hub gene regulatory network can be regarded as key to the understanding COVID-19 infection and its associated complications and might also lead to new therapeutic approaches. hsa-mir-4484 [552], hsa-mir-4511 [553], STAT3 [554], KLF5 [555], SRF (Serum response factor) [556], GATA3 [557] and USF1 [558] [574] and USF1 [575] have been shown to be activated in cardiovascular diseases. hsa-mir-3615 [576], hsamir-1825 [577], STAT3 [578], KLF5 [579], SREBF2 [580], GATA3 [Huda et al 2018] and USF1 [Meex et al 2008] were identified to be closely associated in patients with diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

“…miRNA-hub gene regulatory network and TF-hub gene regulatory network can be regarded as key to the understanding COVID-19 infection and its associated complications and might also lead to new therapeutic approaches. hsa-mir-4484 [552], hsa-mir-4511 [553], STAT3 [554], KLF5 [555], SRF (Serum response factor) [556], GATA3 [557] and USF1 [558] have been implicated as a principal mediator of kidney diseases. Studies have reported that hsa-mir-190b [559], hsamir-4693-5p [560], hsa-mir-1470 [560], hsa-mir-1825 [561], STAT3 [562], SREBF2 [563] and SRF (Serum response factor) [564] are necessary for neurological diseases.…”

Section: Discussionmentioning

confidence: 99%

Screening key genes and signaling pathways in COVID-19 infection and its associated complications by integrated bioinformatics analysis

Vastrad¹,

Vastrad²

2021

Preprint

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Severe acute respiratory syndrome corona virus 2 (SARS-CoV-2)/ coronavirus disease 2019 (COVID-19) infection is the leading cause of respiratory tract infection associated mortality worldwide. The aim of the current investigation was to identify the differentially expressed genes (DEGs) and enriched pathways in COVID-19 infection and its associated complications by bioinformatics analysis, and to provide potential targets for diagnosis and treatment. Valid next-generation sequencing (NGS) data of 93 COVID 19 samples and 100 non COVID 19 samples (GSE156063) were obtained from the Gene Expression Omnibus database. Gene ontology (GO) and REACTOME pathway enrichment analysis was conducted to identify the biological role of DEGs. In addition, a protein-protein interaction network, modules, miRNA-hub gene regulatory network, TF-hub gene regulatory network and receiver operating characteristic curve (ROC) analysis were used to identify the key genes. A total of 738 DEGs were identified, including 415 up regulated genes and 323 down regulated genes. Most of the DEGs were significantly enriched in immune system process, cell communication, immune system and signaling by NTRK1 (TRKA). Through PPI, modules, miRNA-hub gene regulatory network, TF-hub gene regulatory network analysis, ESR1, UBD, FYN, STAT1, ISG15, EGR1, ARRB2, UBE2D1, PRKDC and FOS were selected as hub genes, which were expressed in COVID-19 samples relative to those in non COVID-19 samples, respectively. Among them, ESR1, UBD, FYN, STAT1, ISG15, EGR1, ARRB2, UBE2D1, PRKDC and FOS were suggested to be diagonstic factors for COVID-19. The findings from this bioinformatics analysis study identified molecular mechanisms and the key hub genes that might contribute to COVID-19 infection and its associated complications.

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Complement C5 activation promotes type 2 diabetic kidney disease via activating STAT3 pathway and disrupting the gut‐kidney axis

Cited by 41 publications

References 60 publications

Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes

Pathogenesis and Clinical Significance of In-Stent Restenosis in Patients with Diabetes

Gut microbiota, key to unlocking the door of diabetic kidney disease

Screening key genes and signaling pathways in COVID-19 infection and its associated complications by integrated bioinformatics analysis

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