&lt;p&gt;Circulating Tissue Factor-Positive Procoagulant Microparticles in Patients with Type 1 Diabetes&lt;/p&gt;

Zhang, Chenghui; Ou, Qing; Gu, Yan; Cheng, Gaiping; Du, Rongni; Li, Yuan; Cordiner, Ruth; Kang, Deying; Zhang, Jiaying; Huang, Qiaorong; Yu, Chuan; Li, Kang; Wang, Xuan; Sun, Xin; Mo, Xianming; Tian, Haoming; Pearson, Ewan R.; Wei, Meng; Li, Sheyu

doi:10.2147/dmso.s225761

Cited by 4 publications

(3 citation statements)

References 48 publications

(51 reference statements)

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“…The molecular bridge between hemostasis and the innate inflammatory response is the coagulation trigger, TF. 50 TF has been unequivocally identified as a mechanistic pathophysiological mediator in numerous mouse models of disease and clinical correlations have been made; examples include cancer, 51,52 sickle cell disease, 53,54 obesity and diabetes, [55][56][57] rheumatoid arthritis, 58,59 and cardiovascular disease. 60,61 Thus, TF is a probable effector of the progression and severity of thrombosis and inflammation seen in COVID-19.…”

Section: Tf Connects Coagulation and Inflammationmentioning

confidence: 99%

Antiviral anticoagulation

Pryzdial

Sutherland

Lin

et al. 2020

Research and Practice in Thrombosis and Haemostasis

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Severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) is a novel envelope virus that causes coronavirus disease 2019 (COVID‐19). Hallmarks of COVID‐19 are a puzzling form of thrombophilia that has elevated D‐dimer but only modest effects on other parameters of coagulopathy. This is combined with severe inflammation, often leading to acute respiratory distress and possible lethality. Coagulopathy and inflammation are interconnected by the transmembrane receptor, tissue factor (TF), which initiates blood clotting as a cofactor for factor VIIa (FVIIa)‐mediated factor Xa (FXa) generation. TF also functions from within the nascent TF/FVIIa/FXa complex to trigger profound changes via protease‐activated receptors (PARs) in many cell types, including SARS‐CoV‐2–trophic cells. Therefore, aberrant expression of TF may be the underlying basis of COVID‐19 symptoms. Evidence suggests a correlation between infection with many virus types and development of clotting‐related symptoms, ranging from heart disease to bleeding, depending on the virus. Since numerous cell types express TF and can act as sites for virus replication, a model envelope virus, herpes simplex virus type 1 (HSV1), has been used to investigate the uptake of TF into the envelope. Indeed, HSV1 and other viruses harbor surface TF antigen, which retains clotting and PAR signaling function. Strikingly, envelope TF is essential for HSV1 infection in mice, and the FXa‐directed oral anticoagulant apixaban had remarkable antiviral efficacy. SARS‐CoV‐2 replicates in TF‐bearing epithelial and endothelial cells and may stimulate and integrate host cell TF, like HSV1 and other known coagulopathic viruses. Combined with this possibility, the features of COVID‐19 suggest that it is a TFopathy, and the TF/FVIIa/FXa complex is a feasible therapeutic target.

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Section: Tf Connects Coagulation and Inflammationmentioning

confidence: 99%

Antiviral anticoagulation

Pryzdial

Sutherland

Lin

et al. 2020

Research and Practice in Thrombosis and Haemostasis

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“…We previously revealed the involvement of PAI-1 in delayed bone repair induced by a diabetic state in mice [ 15 – 17 ]. TF antigen levels and the number of TF-positive microvesicles were found to be elevated in the blood of diabetic patients [ 18 , 19 ]. However, it is important to note that several methods may be used to measure plasma TF levels, including antigen- and activity-based assays [ 20 ].…”

Section: Introductionmentioning

confidence: 99%

Role of tissue factor in delayed bone repair induced by diabetic state in mice

et al. 2021

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Background Tissue factor (TF) is the primary activator of the extrinsic coagulation protease cascade. Although TF plays roles in various pathological states, such as thrombosis, inflammatory diseases, cancer, and atherosclerosis, its involvement in bone metabolism remains unknown. Materials and methods The present study examined the roles of TF in delayed bone repair induced by a diabetic state in mice using wild-type (WT) and low TF-expressing (LTF) male mice. A diabetic state was induced by intraperitoneal injections of streptozotocin (STZ). Results A prolonged diabetic state significantly reduced total and trabecular bone mineral densities (BMD) as well as cortical bone thickness in WT and LTF mice; these BMD parameters were similar between WT and LTF mice treated with or without STZ. The diabetic state induced in WT mice delayed the repair of the femur following injury. The diabetic state induced in LTF mice was associated with further delays in bone repair. In in vitro experiments, TF significantly decreased receptor activator of nuclear factor-κB ligand-induced osteoclast formation and osteoclastogenic gene expression in RAW264.7 cells. However, it did not affect the gene expression levels of runt-related transcription factor 2 and osterix as well as alkaline phosphatase activity in mouse primary osteoblasts. Conclusion Low TF state was associated with enhanced bone repair delay induced by diabetic state in mice. The TF-induced suppression of bone remodeling may be a contributing factor to the protective effects of TF against delayed bone repair in a diabetic state.

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“…As a consequence, many diabetic studies have been published during the past few decades [ 6 – 9 ]. Along with the increasing of the literature in original diabetic articles [ 10 , 11 ], the systematic reviews/meta-analyses on diabetic research are also increasing. Assessment quality and quantity of literature has become much more important in the scientific area, and bibliometrics analysis is the most important involved method [ 12 – 14 ].…”

Section: Introductionmentioning

confidence: 99%

The 100 Top-Cited Systematic Reviews/Meta-Analyses on Diabetic Research

Yang

Chen

et al. 2020

Journal of Diabetes Research

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Objective. The objective of this study was to analyze the 100 top-cited systematic reviews/meta-analyses on diabetic research. Methods. The Science Citation Index Expanded database was searched to identify top-cited studies on diabetic research up to March 4th, 2020. Studies were analyzed using the following characteristics: citation number, publication year, country and institution of origin, authorship, topics, and journals. Results. The 100 top-cited diabetic systematic reviews/meta-analyses were published in 43 different journals, with Diabetes Care having the highest numbers (n=17), followed by The Journal of the American Medical Association (n=14) and Lancet (n=9). The majority of studies are published in the 2000s. The number of citations ranged from 2197 to 301. The highest number of contributions was from the USA, followed by England and Australia. The leading institution was Harvard University. The hot topic was a risk factor (n=33), followed by comorbidity (n=27). Conclusions. The 100 top-cited systematic reviews/meta-analyses on diabetic research identify impactful authors, journals, institutes, and countries. It will also provide the most important references to evidence-based medicine in diabetes and serve as a guide to the features of a citable paper in this field.

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<p>Circulating Tissue Factor-Positive Procoagulant Microparticles in Patients with Type 1 Diabetes</p>

Cited by 4 publications

References 48 publications

Antiviral anticoagulation

Antiviral anticoagulation

Role of tissue factor in delayed bone repair induced by diabetic state in mice

The 100 Top-Cited Systematic Reviews/Meta-Analyses on Diabetic Research

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