61 results on '"Cao, Shirong"'
Search Results
52. Corrigendum to “Myeloid cyclooxygenase-2/prostaglandin E2/E-type prostanoid receptor 4 promotes transcription factor MafB-dependent inflammatory resolution in acute kidney injury.” Kidney Int.2022;101:79–91
- Author
-
Pan, Yu, Cao, Shirong, Terker, Andrew S., Tang, Jiaqi, Sasaki, Kensuke, Wang, Yinqiu, Niu, Aolei, Luo, Wentian, Daassi, Dhouha, Fan, Xiaofeng, Wang, Suwan, Wilson, Matthew H., Zhang, Ming-Zhi, and Harris, Raymond C.
- Published
- 2023
- Full Text
- View/download PDF
53. The Potential Role of HMGB1 Release in Peritoneal Dialysis-Related Peritonitis
- Author
-
Cao, Shirong, primary, Li, Shu, additional, Li, Huiyang, additional, Xiong, Liping, additional, Zhou, Yi, additional, Fan, Jinjin, additional, Yu, Xueqing, additional, and Mao, Haiping, additional
- Published
- 2013
- Full Text
- View/download PDF
54. Atg5-mediated autophagy deficiency in proximal tubules promotes cell cycle G 2 /M arrest and renal fibrosis.
- Author
-
Li, Huiyan, Peng, Xuan, Wang, Yating, Cao, Shirong, Xiong, Liping, Fan, Jinjin, Wang, Yihan, Zhuang, Shougang, Yu, Xueqing, and Mao, Haiping
- Published
- 2016
- Full Text
- View/download PDF
55. Association of Body Mass Index and Body Mass Index Change with Mortality in Incident Peritoneal Dialysis Patients
- Author
-
Xiong, Liping, Cao, Shirong, Xu, Fenghua, Zhou, Qian, Fan, Li, Xu, Qingdong, Mao, Haiping, and Yu, Xueqing
- Published
- 2015
- Full Text
- View/download PDF
56. Analytical and Experimental Investigation of Perforation Layout Parameters on Hydraulic Fracture Propagation
- Author
-
Zuo, Shaojie, Ge, Zhaolong, Lu, Yiyu, Cao, Shirong, and Zhang, Liang
- Abstract
Horizontal wellbore fracturing technology is an effective method to stimulate reservoirs and increase energy production, such as gas, oil, and geothermy. The perforation layout parameters are the key parameters affecting the fracturing effect. To analyze the influence of perforation layout parameters on hydraulic fracture propagation and optimization of the perforation layout parameters, the stress surrounding the perforation is derived, key oriented points and effective oriented angles are defined, and effective oriented criteria are proposed. The principal stress direction angle can be divided into three stages as the distance from the fracturing hole increases: decreasing stage (tends to the connection direction of perforations), stable stage, and increasing stage (tends to the maximum horizontal ground stress direction). A common relationship between the perforation length, the initial angle, the ground stress difference, and the suitable oriented angle is obtained. The results will guide the field application of the above fracturing technologies.
- Published
- 2021
- Full Text
- View/download PDF
57. Cyclooxygenase-2 in adipose tissue macrophages limits adipose tissue dysfunction in obese mice.
- Author
-
Yu Pan, Shirong Cao, Jiaqi Tang, Arroyo, Juan P., Terker, Andrew S., Yinqiu Wang, Aolei Niu, Xiaofeng Fan, Suwan Wang, Yahua Zhang, Ming Jiang, Wasserman, David H., Ming-Zhi Zhang, Harris, Raymond C., Pan, Yu, Cao, Shirong, Tang, Jiaqi, Wang, Yinqiu, Niu, Aolei, and Fan, Xiaofeng
- Subjects
- *
GLUCOSE metabolism , *OBESITY , *INFLAMMATION , *DINOPROSTONE , *MACROPHAGES , *RESEARCH funding , *OXIDOREDUCTASES , *INSULIN resistance , *MICE , *ADIPOSE tissues , *ANIMALS - Abstract
Obesity-associated complications are causing increasing morbidity and mortality worldwide. Expansion of adipose tissue in obesity leads to a state of low-grade chronic inflammation and dysregulated metabolism, resulting in insulin resistance and metabolic syndrome. Adipose tissue macrophages (ATMs) accumulate in obesity and are a source of proinflammatory cytokines that further aggravate adipocyte dysfunction. Macrophages are rich sources of cyclooxygenase (COX), the rate limiting enzyme for prostaglandin E2 (PGE2) production. When mice were fed a high-fat diet (HFD), ATMs increased expression of COX-2. Selective myeloid cell COX-2 deletion resulted in increased monocyte recruitment and proliferation of ATMs, leading to increased proinflammatory ATMs with decreased phagocytic ability. There were increased weight gain and adiposity, decreased peripheral insulin sensitivity and glucose utilization, increased adipose tissue inflammation and fibrosis, and abnormal adipose tissue angiogenesis. HFD pair-feeding led to similar increases in body weight, but mice with selective myeloid cell COX-2 still exhibited decreased peripheral insulin sensitivity and glucose utilization. Selective myeloid deletion of the macrophage PGE2 receptor subtype, EP4, produced a similar phenotype, and a selective EP4 agonist ameliorated the metabolic abnormalities seen with ATM COX-2 deletion. Therefore, these studies demonstrated that an ATM COX-2/PGE2/EP4 axis plays an important role in inhibiting adipose tissue dysfunction. [ABSTRACT FROM AUTHOR]
- Published
- 2022
- Full Text
- View/download PDF
58. Clonal hematopoiesis of indeterminate potential contributes to accelerated chronic kidney disease progression.
- Author
-
Vlasschaert C, Pan Y, Chen J, Akwo E, Rao V, Hixson JE, Chong M, Uddin MM, Yu Z, Jiang M, Peng F, Cao S, Wang Y, Kim DK, Hung AM, He J, Tamura MK, Cohen DL, He J, Li C, Bhat Z, Rao P, Xie D, Bick AG, Kestenbaum B, Paré G, Rauh MJ, Levin A, Natarajan P, Lash JP, Zhang MZ, Harris RC, Robinson-Cohen C, Lanktree MB, and Kelly TN
- Abstract
Background: Clonal hematopoiesis of indeterminate potential (CHIP) is a common inflammatory condition of aging that causes myriad end-organ damage. We have recently shown associations for CHIP with acute kidney injury and with kidney function decline in the general population, with stronger associations for CHIP driven by mutations in genes other than DNMT3A (non- DNMT3A CHIP). Longitudinal kidney function endpoints in individuals with pre-existing chronic kidney disease (CKD) and CHIP have been examined in two previous studies, which reported conflicting findings and were limited by small sample sizes., Methods: In this study, we examined the prospective associations between CHIP and CKD progression events in four cohorts of CKD patients (total N = 5,772). The primary outcome was a composite of 50% kidney function decline or kidney failure. The slope of eGFR decline was examined as a secondary outcome. Mendelian randomization techniques were then used to investigate potential causal effects of CHIP on eGFR decline. Finally, kidney function was assessed in adenine-fed CKD model mice having received a bone marrow transplant recapitulating Tet2 -CHIP compared to controls transplanted wild-type bone marrow., Results: Across all cohorts, the average age was 66.4 years, the average baseline eGFR was 42.6 ml/min/1.73m
2 , and 24% had CHIP. Upon meta-analysis, non- DNMT3A CHIP was associated with a 59% higher relative risk of incident CKD progression (HR 1.59, 95% CI: 1.02-2.47). This association was more pronounced among individuals with diabetes (HR 1.29, 95% CI: 1.03-1.62) and with baseline eGFR ≥ 30 ml/min/1.73m (HR 1.80, 95% CI: 1.11-2.90). Additionally, the annualized slope of eGFR decline was steeper among non- DNMT3A CHIP carriers, relative to non-carriers (β -0.61 ± 0.31 ml/min/1.73m2 , p = 0.04). Mendelian randomization analyses suggested a causal role for CHIP in eGFR decline among individuals with diabetes. In a dietary adenine mouse model of CKD, Tet2 -CHIP was associated with lower GFR as well as greater kidney inflammation, tubular injury, and tubulointerstitial fibrosis., Conclusion: Non- DNMT3A CHIP is a potentially targetable novel risk factor for CKD progression.- Published
- 2024
- Full Text
- View/download PDF
59. Role of protease-activated receptor 4 in mouse models of acute and chronic kidney injury.
- Author
-
Erreger K, Cao S, Pan Y, Jiang M, Zhang MZ, Harris RC, and Hamm HE
- Subjects
- Animals, Mice, Endothelial Cells metabolism, Fibrosis, Inflammation pathology, Ischemia pathology, Kidney metabolism, Mice, Knockout, Receptors, Thrombin genetics, Receptors, Thrombin metabolism, Reperfusion Injury pathology, Thrombin metabolism, Thrombin pharmacology, Acute Kidney Injury genetics, Acute Kidney Injury pathology, Renal Insufficiency, Chronic genetics, Renal Insufficiency, Chronic pathology
- Abstract
Protease-activated receptor 4 (PAR4) is a G protein-coupled receptor activated by thrombin. In the platelet, response to thrombin PAR4 contributes to the predominant procoagulant microparticle formation, increased fibrin deposition, and initiation of platelet-stimulated inflammation. In addition, PAR4 is expressed in other cell types, including endothelial cells. Under inflammatory conditions, PAR4 is overexpressed via epigenetic demethylation of the PAR4 gene, F2RL3 . PAR4 knockout (KO) studies have determined a role for PAR4 in ischemia-reperfusion injury in the brain, and PAR4 KO mice display normal cardiac function but present less myocyte death and cardiac dysfunction in response to acute myocardial infarction. Although PAR4 has been reported to be expressed within the kidney, the contribution of PAR4 to acute kidney injury (AKI) and chronic kidney disease (CKD) is not well understood. Here we report that PAR4 KO mice are protected against kidney injury in two mouse models. First, PAR4 KO mice are protected against induction of markers of both fibrosis and inflammation in two different models of kidney injury: 1 ) 7 days following unilateral ureter obstruction (UUO) and 2 ) an AKI-CKD model of ischemia-reperfusion followed by 8 days of contralateral nephrectomy. We further show that PAR4 expression in the kidney is low in the control mouse kidney but induced over time following UUO. PAR4 KO mice are protected against blood urea nitrogen (BUN) and glomerular filtration rate (GFR) kidney function pathologies in the AKI-CKD model. Following the AKI-CKD model, PAR4 is expressed in the collecting duct colocalizing with Dolichos biflorus agglutinin (DBA), but not in the proximal tubule with Lotus tetragonolobus lectin (LTL). Collectively, the results reported in this study implicate PAR4 as contributing to the pathology in mouse models of acute and chronic kidney injury. NEW & NOTEWORTHY The contribution of the thrombin receptor protease-activated receptor 4 (PAR4) to acute kidney injury (AKI) and chronic kidney disease (CKD) is not well understood. Here we report that PAR4 expression is upregulated after kidney injury and PAR4 knockout (KO) mice are protected against fibrosis following kidney injury in two mouse models. First, PAR4 KO mice are protected against unilateral ureter obstruction. Second, PAR4 KO mice are protected against an AKI-CKD model of ischemia-reperfusion followed by contralateral nephrectomy.
- Published
- 2024
- Full Text
- View/download PDF
60. Clonal Hematopoiesis of Indeterminate Potential is Associated with Acute Kidney Injury.
- Author
-
Vlasschaert C, Robinson-Cohen C, Kestenbaum B, Silver SA, Chen JC, Akwo E, Bhatraju PK, Zhang MZ, Cao S, Jiang M, Wang Y, Niu A, Siew E, Kramer HJ, Kottgen A, Franceschini N, Psaty BM, Tracy RP, Alonso A, Arking DE, Coresh J, Ballantyne CM, Boerwinkle E, Grams M, Lanktree MB, Rauh MJ, Harris RC Jr, and Bick AG
- Abstract
Age is a predominant risk factor for acute kidney injury (AKI), yet the biological mechanisms underlying this risk are largely unknown and to date no genetic mechanisms for AKI have been established. Clonal hematopoiesis of indeterminate potential (CHIP) is a recently recognized biological mechanism conferring risk of several chronic aging diseases including cardiovascular disease, pulmonary disease and liver disease. In CHIP, blood stem cells acquire mutations in myeloid cancer driver genes such as DNMT3A, TET2, ASXL1 and JAK2 and the myeloid progeny of these mutated cells contribute to end-organ damage through inflammatory dysregulation. We sought to establish whether CHIP causes acute kidney injury (AKI). To address this question, we first evaluated associations with incident AKI events in three population-based epidemiology cohorts (N = 442,153). We found that CHIP was associated with a greater risk of AKI (adjusted HR 1.26, 95% CI: 1.19-1.34, p<0.0001), which was more pronounced in patients with AKI requiring dialysis (adjusted HR 1.65, 95% CI: 1.24-2.20, p=0.001). The risk was particularly high in the subset of individuals where CHIP was driven by mutations in genes other than DNMT3A (HR: 1.49, 95% CI: 1.37-1.61, p<0.0001). We then examined the association between CHIP and recovery from AKI in the ASSESS-AKI cohort and identified that non- DNMT3A CHIP was more common among those with a non-resolving pattern of injury (HR 2.3, 95% CI: 1.14-4.64, p = 0.03). To gain mechanistic insight, we evaluated the role of Tet2 -CHIP to AKI in ischemia-reperfusion injury (IRI) and unilateral ureteral obstruction (UUO) mouse models. In both models, we observed more severe AKI and greater post-AKI kidney fibrosis in Tet2 -CHIP mice. Kidney macrophage infiltration was markedly increased in Tet2 -CHIP mice and Tet2 -CHIP mutant renal macrophages displayed greater proinflammatory responses. In summary, this work establishes CHIP as a genetic mechanism conferring risk of AKI and impaired kidney function recovery following AKI via an aberrant inflammatory response in CHIP derived renal macrophages.
- Published
- 2023
- Full Text
- View/download PDF
61. Association of Pulmonary Hypertension with Mortality in Incident Peritoneal Dialysis Patients.
- Author
-
Xu Q, Xiong L, Fan L, Xu F, Yang Y, Li H, Peng X, Cao S, Zheng Z, Yang X, Yu X, and Mao H
- Subjects
- Adult, Aged, Cause of Death, Echocardiography, Female, Follow-Up Studies, Humans, Kaplan-Meier Estimate, Kidney Failure, Chronic mortality, Kidney Failure, Chronic therapy, Male, Middle Aged, Prevalence, Prognosis, Retrospective Studies, Risk Assessment, Risk Factors, Hypertension, Pulmonary mortality, Peritoneal Dialysis mortality
- Abstract
Background: The prognostic value of pulmonary hypertension at the start of peritoneal dialysis (PD) in patient survival is unclear., Methods: We conducted a retrospective study of incident patients who initiated PD therapy from January 2007 to December 2011, and followed up through June 2013. Pulmonary hypertension was defined as an estimated systolic pulmonary artery pressure (PAP) of ≥ 35 mm Hg using echocardiography. Clinical parameters and laboratory findings were compared between patients with and without pulmonary hypertension and a logistic regression model was elaborated. Patient outcomes (all-cause and cardiovascular mortality) were recorded during follow-up. Survival curves were constructed by the Kaplan-Meier method, and the influences of pulmonary hypertension on outcomes were analyzed by Cox regression models., Results: Pulmonary hypertension was prevalent in 99 (16.0%) of the 618 patients studied. The independent risk factors for pulmonary hypertension were female (odds ratio [OR] = 2.12; 95% confidence interval [CI]: 1.29 - 3.46), left atrial diameter (OR = 1.15; 95% CI: 1.10 - 1.20), left ventricular ejection fraction (OR = 0.97; 95% CI: 0.95 - 0.99), and serum sodium (OR = 0.94; 95% CI: 0.89 - 0.99). Over a median follow-up of 29.4 months, 93 patients (15.0%) died, 59.1% of them due to cardiovascular disease. Kaplan-Meier survival analysis showed that patients with pulmonary hypertension had worse overall rates of survival and cardiovascular death-free survival than those without pulmonary hypertension. After multivariate adjustment, pulmonary hypertension was independently associated with increased risk for both all-cause and cardiovascular mortality, with hazard ratios (HRs) of 2.10 (95% CI: 1.35 - 3.27) and 2.60 (95% CI: 1.48 - 4.56), respectively., Conclusions: The prevalence of pulmonary hypertension at the start of PD was common and associated with increased risk of both all-cause and cardiovascular mortality in incident PD patients., (Copyright © 2015 International Society for Peritoneal Dialysis.)
- Published
- 2015
- Full Text
- View/download PDF
Catalog
Discovery Service for Jio Institute Digital Library
For full access to our library's resources, please sign in.