ORCID Profile
0000-0002-7889-1697
Current Organisations
Anhui Provincial Hospital
,
Deakin University
,
The First Affiliated Hospital, Division of Life Sciences and Medicine, University of Science and Technology of China
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Publisher: Wiley
Date: 19-02-2015
Publisher: Springer Science and Business Media LLC
Date: 19-01-2022
Publisher: American Physical Society (APS)
Date: 19-05-2023
Publisher: Elsevier BV
Date: 07-2011
DOI: 10.1016/J.EXPNEUROL.2010.04.006
Abstract: Statins have been widely used for the treatment of a variety of conditions beyond their original role in lowering cholesterol. Since statins have relatively few side effects, they have been recognized as useful medicine to ameliorate neurodegenerative disorders. Current studies on the applications of statins have demonstrated their neuroprotective and clinical significance among neurodegenerative diseases like cerebral ischemic stroke, vascular dementia, Alzheimer's disease, and Parkinson's disease, though the neuroprotective mechanisms are not completely understood. This review will discuss recent development in the use of statins in slowing down the progression of these neurodegenerative diseases. It will summarize the potential mechanisms for statin-mediated neuroprotective effects in neurodegenerative diseases. In detail, this review discuss the roles of statins in lowering cholesterol, reducing reactive oxygen species, impairing β-amyloid production and serum apolipoprotein E levels, enhancing the levels of endothelial nitric oxide synthase and cerebral blood flow, and modulating cognitive related receptors and matrix metalloproteases. Finally, different alterations of various receptors in brain regions following statin treatment and their correlations with cognitive dysfunction in Parkinson's disease will also be reviewed, as well as the potential for therapy in ameliorating the progression of Parkinson's disease. This article is part of a Special Issue entitled "Interaction between repair, disease, & inflammation."
Publisher: American Society for Pharmacology & Experimental Therapeutics (ASPET)
Date: 04-06-2021
Publisher: IOP Publishing
Date: 23-05-2018
Publisher: Wiley
Date: 29-05-2020
Publisher: Springer Science and Business Media LLC
Date: 27-05-2023
DOI: 10.1038/S41392-023-01439-Y
Abstract: The ever-increasing prevalence of noncommunicable diseases (NCDs) represents a major public health burden worldwide. The most common form of NCD is metabolic diseases, which affect people of all ages and usually manifest their pathobiology through life-threatening cardiovascular complications. A comprehensive understanding of the pathobiology of metabolic diseases will generate novel targets for improved therapies across the common metabolic spectrum. Protein posttranslational modification (PTM) is an important term that refers to biochemical modification of specific amino acid residues in target proteins, which immensely increases the functional ersity of the proteome. The range of PTMs includes phosphorylation, acetylation, methylation, ubiquitination, SUMOylation, neddylation, glycosylation, palmitoylation, myristoylation, prenylation, cholesterylation, glutathionylation, S-nitrosylation, sulfhydration, citrullination, ADP ribosylation, and several novel PTMs. Here, we offer a comprehensive review of PTMs and their roles in common metabolic diseases and pathological consequences, including diabetes, obesity, fatty liver diseases, hyperlipidemia, and atherosclerosis. Building upon this framework, we afford a through description of proteins and pathways involved in metabolic diseases by focusing on PTM-based protein modifications, showcase the pharmaceutical intervention of PTMs in preclinical studies and clinical trials, and offer future perspectives. Fundamental research defining the mechanisms whereby PTMs of proteins regulate metabolic diseases will open new avenues for therapeutic intervention.
Publisher: Wiley
Date: 03-04-2017
DOI: 10.1111/DOM.12920
Abstract: To compare glucose control and safety of different basal insulin therapies (BI, including Insulin NPH, glargine and detemir) in real-world clinical settings based on a large-scale registry study. In this multi-center 6-month prospective observational study, patients with type 2 diabetes (HbA1c ≥ 7%) who were uncontrolled by oral anti-diabetic drugs (OADs) and were willing to initiate BI therapy were enrolled from 209 hospitals within 8 regions of China. Type and dose of BI were at the physician's discretion and the patients' willingness. Interviews were conducted at 0 months (visit 1), 3 months (visit 2) and 6 months (visit 3). Outcomes included change in HbA1c, hypoglycemia rate and body weight from baseline at 6 months. A total of 16 341 and 9002 subjects were involved in Intention-To-Treat (ITT) and per-protocol (PP) analysis, respectively. After PS regression adjustment, ITT analysis showed that reduction in HbA1c in glargine (2.2% ± 2.1%) and detemir groups (2.2% ± 2.1%) was higher than that in the NPH group (2.0% ± 2.2%) (P < .01). The detemir group had the lowest weight gain (-0.1 ± 2.9 kg) compared with the glargine (+0.1 ± 3.0 kg) and NPH (+0.3 ± 3.1 kg) groups (P < .05). The glargine group had the lowest rate of minor hypoglycaemia, while there was no difference in severe hypoglycaemia among the 3 groups. The results observed in PP analyses were consistent with those in ITT analysis. In a real-world clinical setting in China, treatment with long-acting insulin analogues was associated with better glycaemic control, as well as less hypoglycaemia and weight gain than treatment with NPH insulin in type 2 diabetes patients. However, the clinical relevance of these observations must be interpreted with caution.
Publisher: Elsevier BV
Date: 09-2023
Publisher: Wiley
Date: 17-03-2017
DOI: 10.1111/DOM.12886
Abstract: To examine treatment patterns following basal insulin (BI) introduction in type 2 diabetes mellitus (T2DM) patients under real-world conditions across China. Overall, 18 995 patients inadequately controlled (HbA1c ≥ 53 mmol/mol [7%]) with oral antihyperglycaemic drugs (OADs) and willing to receive BI treatment were registered at 209 hospitals and followed at baseline (visit 1), 3 months (visit 2) and 6 months (visit 3). Type of BI was initiated at physicians' discretion. Retention with BI therapy at 6 months was 75.6%. Use of long-acting BI predominated, with insulin glargine accounting for 71%, detemir 13% and Neutral Protamine Hagedorn (NPH) insulin 16%. Over 70% of long-acting users maintained the same initial BI at visit 3, while 40% of NPH users switched treatment and 24.4% of participants initiated BI with prandial insulin. The initial mean (± SD) dose of BI and total insulin was 0.18 ± 0.07 and 0.25 ± 0.19 IU/kg, respectively, with a mean increase of daily dose by 0.03 and 0.02 IU/kg after 6 months, respectively. Only 56.6% of insulin users reported dose titration at visit 3. Mean HbA1c was 81 mmol/mol (9.6%) at baseline and 57 mmol/mol (7.4%) at 6 months. The frequency of hypoglycaemia was 1.61 and 2.07 episodes atient-year at baseline and 6 months, respectively. In real-world clinical settings, add-on BI therapy in T2DM patients is associated with significant improvement in glycaemic control without overtly compromising safety related to hypoglycaemia and weight gain. Evolution of insulin treatment regimens varied among patients, but dose titration was suboptimal. More active BI dose titration might further improve glycaemic outcome in patients receiving BI therapy. A free Video Abstract to accompany this article is available at 12655959.
Publisher: American Physical Society (APS)
Date: 22-12-2021
Publisher: American Physical Society (APS)
Date: 24-07-2019
Publisher: Mary Ann Liebert Inc
Date: 10-2015
Abstract: Efficacy of basal insulin (BI) has been well studied by randomized controlled trials, but the impact of BI on glycemic control in the real world has not been well documented. The Observational Registry for BI Treatment (ORBIT) study is designed to evaluate the real-life outcomes of BI in China. Participants with type 2 diabetes (n=19,894), from December 2011 to June 2013, inadequately controlled on oral hypoglycemic agents (OHAs) were initiated on BI treatment from 209 hospitals in all the eight regions in Mainland China. Data for each patient on use of OHAs and insulin (type and dose), glycemic control, hypoglycemic episodes, body weight, quality of life, and costs were collected at baseline and 3 and 6 months. For the 18,995 participants who were eligible for baseline analysis, mean±SD age was 55.4±10.4 years, with 52.5% males. The mean duration of diabetes was 6.4±5.3 years and was positively associated with the economic level of eight regions. Before initiation of BI, patients had a mean hemoglobin A1c level of 9.6±2.0% with a fasting plasma glucose level of 11.7±4.0 mmol/L. Of the patients, 35.5% had some diabetes complications. Metformin, sulfonylureas, and α-glycosidase inhibitors were the most commonly used OHAs. The proportions of patients using one, two, or more than two OHAs before BI initiation were 48.4%, 42.7%, and 8.9%, respectively. To the best of our knowledge, the ORBIT study is the largest registry study to evaluate glycemic outcomes and safety of BI in real-world China. Baseline data indicate delays in initiation of BI in the majority of patients with type 2 diabetes in China.
Publisher: American Physical Society (APS)
Date: 31-07-2018
Publisher: Elsevier BV
Date: 07-2017
DOI: 10.1016/J.DIABRES.2017.02.027
Abstract: The paucity of data on Type 1 diabetes in China hinders progress in care and policy-making. This study compares Type 1 diabetes care and clinical outcomes in Beijing and Shantou with current clinical guidelines. The 3C Study was a cross-sectional study of the clinical practices and outcomes of people with Type 1 diabetes. The study sequentially enrolled 849 participants from hospital records, inpatient wards, and outpatient clinics. Data were collected via face-to-face interviews with patients and health professionals, the Summary of Diabetes Self-Care Activities, medical records, and venous blood s les. Care was audited using ISPAD/IDF indicators. Data underwent descriptive analysis and tests for association. The median age was 22years (IQR=13-34years), and 48.4% of the s le had diabetes less than six years. The median HbA1c was 8.5% (69mmol/mol) (IQR 7.2-10.5%), with significant regional variance (p=0.002). Insulin treatment was predominantly two injections/day (45% of patients). The highest incidence of diabetic ketoacidosis was 14.4 events/100 patient years among adolescents. Of the 57.3% of patients with LDL-C>2.6mmol/L, only 11.2% received treatment. Of the 10.6% considered hypertensive, 47.1% received treatment. Rates of documented screening for retinopathy, nephropathy, and peripheral neuropathy were 35.2%, 42.3%, and 25.0%, respectively. The median number of days of self-monitoring/week was 3.0 (IQR=1.0-7.0). There were significant differences in care practices across regions. The study documented an overall deficit in care with significant regional differences noted compared to practice guidelines. Modifications to treatment modalities and the structure of care may improve outcomes.
Publisher: MDPI AG
Date: 14-12-2021
DOI: 10.3390/BIOMEDICINES9121908
Abstract: There is emerging evidence of an association between epigenetic modifications, glycemic control and atherosclerosis risk. In this study, we mapped genome-wide epigenetic changes in patients with type 2 diabetes (T2D) and advanced atherosclerotic disease. We performed chromatin immunoprecipitation sequencing (ChIP-seq) using a histone 3 lysine 9 acetylation (H3K9ac) mark in peripheral blood mononuclear cells from patients with atherosclerosis with T2D (n = 8) or without T2D (ND, n = 10). We mapped epigenome changes and identified 23,394 and 13,133 peaks in ND and T2D in iduals, respectively. Out of all the peaks, 753 domains near the transcription start site (TSS) were unique to T2D. We found that T2D in atherosclerosis leads to an H3K9ac increase in 118, and loss in 63 genomic regions. Furthermore, we discovered an association between the genomic locations of significant H3K9ac changes with genetic variants identified in previous T2D GWAS. The transcription factor 7-like 2 (TCF7L2) rs7903146, together with several human leukocyte antigen (HLA) variants, were among the domains with the most dramatic changes of H3K9ac enrichments. Pathway analysis revealed multiple activated pathways involved in immunity, including type 1 diabetes. Our results present novel evidence on the interaction between genetics and epigenetics, as well as epigenetic changes related to immunity in patients with T2D and advanced atherosclerotic disease.
Publisher: Springer Science and Business Media LLC
Date: 12-07-2021
DOI: 10.1038/S41392-021-00690-5
Abstract: Coronavirus disease 2019 (COVID-19) is regarded as an endothelial disease (endothelialitis) with its patho-mechanism being incompletely understood. Emerging evidence has demonstrated that endothelial dysfunction precipitates COVID-19 and its accompanying multi-organ injuries. Thus, pharmacotherapies targeting endothelial dysfunction have potential to ameliorate COVID-19 and its cardiovascular complications. The objective of the present study is to evaluate whether kruppel-like factor 2 (KLF2), a master regulator of vascular homeostasis, represents a therapeutic target for COVID-19-induced endothelial dysfunction. Here, we demonstrate that the expression of KLF2 was reduced and monocyte adhesion was increased in endothelial cells treated with COVID-19 patient serum due to elevated levels of pro-adhesive molecules, ICAM1 and VCAM1. IL-1β and TNF-α, two cytokines elevated in cytokine release syndrome in COVID-19 patients, decreased KLF2 gene expression. Pharmacologic (atorvastatin and tannic acid) and genetic (adenoviral overexpression) approaches to augment KLF2 levels attenuated COVID-19-serum-induced increase in endothelial inflammation and monocyte adhesion. Next-generation RNA-sequencing data showed that atorvastatin treatment leads to a cardiovascular protective transcriptome associated with improved endothelial function (vasodilation, anti-inflammation, antioxidant status, anti-thrombosis/-coagulation, anti-fibrosis, and reduced angiogenesis). Finally, knockdown of KLF2 partially reversed the ameliorative effect of atorvastatin on COVID-19-serum-induced endothelial inflammation and monocyte adhesion. Collectively, the present study implicates loss of KLF2 as an important molecular event in the development of COVID-19-induced vascular disease and suggests that efforts to augment KLF2 levels may be therapeutically beneficial.
Location: China
No related grants have been discovered for Jianping Weng.