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Traditional Medicine Research 2024年第9期9卷 21-31页

作者： Han-Qing Zhang Shuang Wu Xin Chen Ya-Xuan Fang Qiu-Mei Lan Zi-Jun Zhou Yan-Heng Qiao Jie Li Yan-Ru Zhao Ming Pei Bo Yang Department of Nephropathy First Teaching Hospital of Tianjin University of Traditional Chinese MedicineTianjin 300381China National Clinical Research Center for Chinese Medicine Acupuncture and Moxibustion Tianjin 300381China

vascular calcification is a crucial risk factor that affects the incidence and mortality of cardiovascular disease in chronic kidney disease patients.Modern medicine relies on calcium-phosphorus binding agents,calcium mimetics,active vitamin D,and hemodialysis to prevent and treat vascular calcification,however,their efficacy is unsatisfactory and adverse reactions often occur.Medical plant therapy can act as an integrative regulator in patients with chronic kidney disease-associated vascular calcification,which can significantly improve patients’symptoms,but its specific mechanism has not been fully elucidated yet.In this paper,we reviewed the domestic and international theoretical studies on the pathogenesis mechanism of chronic kidney disease-associated vascular calcification in recent years,summarized eight active ingredients of medicinal plants as well as four compound formulas for improving chronic kidney disease-associated vascular calcification,and explored the mechanism of action of herbal medicine,which will provide a new strategy for promoting the prevention and treatment of vascular calcification.

关键词： chronic kidney disease chronic kidney disease-mineral and bone disorder(CKD-MBD) vascular calcification medicinal plants herbal monomers

Nano-hydroxyapatite accelerates vascular calcification via lysosome impairment and autophagy dysfunction in smooth muscle cells

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Bioactive Materials 2022年第2期7卷 478-493页

作者： Qi Liu Yi Luo Yun Zhao Pingping Xiang Jinyun Zhu Wangwei Jing Wenjing Jin Mingyao Chen Ruikang Tang Hong Yu Department of Cardiology Cardiovascular Key Laboratory of Zhejiang ProvinceThe Second Affiliated HospitalZhejiang University School of MedicineHangzhouZhejiang Province310009China The Affiliated Cardiovascular Hospital of Qingdao University QingdaoShandong Province266071China Department of Chemistry Zhejiang UniversityHangzhouZhejiang Province310027China

vascular calcification(VC)is a common characteristic of aging,diabetes,chronic renal failure,and atherosclerosis.The basic component of VC is hydroxyapatite(HAp).Nano-sized HAp(nHAp)has been identified to play an essential role in the development of pathological calcification of vasculature.However,whether nHAp can induce calcification in vivo and the mechanism of nHAp in the progression of VC remains unclear.We discovered that nHAp existed both in vascular smooth muscle cells(VSMCs)and their extracellular matrix(ECM)in the calcified arteries from patients.Synthetic nHAp had similar morphological and chemical properties as natural nHAp recovered from calcified artery.nHAp stimulated osteogenic differentiation and accelerated mineralization of VSMCs in vitro.Synthetic nHAp could also directly induce VC in vivo.Mechanistically,nHAp was internalized into lysosome,which impaired lysosome vacuolar H+-ATPase for its acidification,therefore blocked autophagic flux in VSMCs.Lysosomal re-acidification by cyclic-3′,5′-adenosine monophosphate(cAMP)significantly enhanced autophagic degradation and attenuated nHAp-induced calcification.The accumulated autophagosomes and autolysosomes were converted into calcium-containing exosomes which were secreted into ECM and accelerated vascular calcium deposit.Inhibition of exosome release in VSMCs decreased calcium deposition.Altogether,our results demonstrated a repressive effect of nHAp on lysosomal acidification,which inhibited autophagic degradation and promoted a conversion of the accumulated autophagic vacuoles into exosomes that were loaded with undissolved nHAp,Ca^(2+),Pi and ALP.These exosomes bud off the plasma membrane,deposit within ECM,and form calcium nodules.vascular calcification was thus accelerated by nHAP through blockage of autophagic flux in VSMCs.

关键词： Nano-hydroxyapatite vascular calcification Autophagy Lysosome Exosome

vascular calcification： Current Genetics Underlying This Complex Phenomenon

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Chinese Medical Journal 2017年第9期130卷 1113-1121页

作者： Nonanzit Perez-Hernandez Gad Aptilon-Duque Ruben Blachman-Braun Gilberto Vargas-Alarcon Adrian Asael Rodriguez-Cortes Shely Azrad-Daniez Rosalinda Posadas-Sanchez Jose Manuel Rodriguez-Perez Department of Molecular Biology National Institute of Cardiology "lgnacio Chavez" Mexico Mexico City 14080 Mexico 2Department of Endocrinology National Institute of Cardiology "Ignacio Chavez" Mexico Mexico City 14080 Mexico

Objective： vascular calcification is the consequence of the complex interaction between genetic, environmental, and vascular factors, which ultimately lead to the deposition of calcium in the tunica intima （atherosclerotic calcification） or tunica media （M6nckenberg＇s sclerosis）. vascular calcification is also closely related to other pathologies, such as diabetes mellitus, dyslipidemia, and chronic kidney disease. It has been concluded that the degree of vascular calcification may vary from person to person, even if the associated pathologies and environmental factors are the same. Therefore, this suggests an important genetic contribution to the development of vascular calcification. This review aimed to find the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways. Data Sources： We conducted an exhaustive search in Scopus, EBSCO, and PubMed with the keywords ＂genetics and vascular calcification＂, ＂molecular pathways, genetic and vascular calcification＂ and included the main articles from January 1995 up to August 2016. We focused on the most recent evidence about vascular calcification pathophysiology regarding the genetic aspects and molecular pathways. Study Selection： The most valuable published original and review articles related to our objective were selected. Results： vascular calcification is a multifactorial disease; thus, its pathophysiology cannot be explained by a single specific factor, rather than by the result of the association of several genetic variants, molecular pathway interactions, and environmental factors that promote its development. Conclusion： Although several molecular aspects of this mechanism have been elucidated, there is still a need for a better understanding of the factors that predispose to this disease.

关键词： Atherosclerosis Cardiovascular Risk Genetics Polymorphisms vascular calcification

Protection Effect of Exogenous Fibroblast Growth Factor 21 on the Kidney Injury in vascular calcification Rats

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Chinese Medical Journal 2018年第5期131卷 532-538页

作者： Yu-Chen Shi Wei-Wei Lu Yue-Long Hou Kun Fu Feng Gan Shu-Juan Cheng Shao-Ping Wang Yong-Fen Qi Jing-Hua Liu Department of Cardiology Beijing Anzhen Hospital Capital Medical University and Beijing Institute of Heart Lung and Blood Vessel Diseases Beijing 100029 China Department of Physiology Xuzhou Medical University Xuzhou Jiangsu 221004 China Department of Pharmacology and Nutritional Sciences University of Kentucky Lexington Kentucky USA Key Laboratory of Molecular Cardiovascular Science Ministry of Education Peking University Health Science Center Beijing 100191 China Department of Cardiology Beijing Aerospace General Hospital Beijing 100076 China

Background： Chronic kidney disease （CKD） is closely related to the cardiovascular events in vascular calcification （VC）. However, little has known about the characteristics of kidney injury caused by VC. Fibroblast growth factor 21 （FGF21 ） is an endocrine thctor, which takes part in various metabolic actions with the potential to alleviate metabolic disorder diseases, Even FGF21 has been regarded as a biomarker in CKD, the role of FGF21 in CKD remains unclear. Therefore, in this study, we evaluate the FGF21 on the kidney injury in VC rats. Methods： The male Sprague-Dawley rats were divided into three groups：（ 1 ） control group, （2） Vitamin D3 plus nicotine （VDN）-induced VC group, （3） FGF21-treated VDN group. After 4 weeks, the rats were killed and the blood was collected for serum creatinine, urea nitrogen, calcium, and phosphate measurement. Moreover, the renal tissues were homogenized for alkaline phosphatases （ALPs） activity and calcium content. The levels of FGF21 protein were measured by radioimmunoassay. The levels of β-Klotho and FGF receptor 1 （FGFR1） protein were measured by enzyme-linked immunosorbent assay （EL1SA）. The structural damage and calcifications in aortas were stained by Alizarin-red S. Moreover, the structure of kidney was observed by hematoxylin and eosin staining. Results： The renal lhnction impairment caused by VDN modeling was ameliorated by FGF21 treatment, inhibited the elevated serum creatinine and urea level by 20.5% （34.750 ± 4.334 pmol/L vs. 27.630± 2.387pamol/L） and 4.0% （7.038 ± 0.590 mmol/L vs. 6.763 ±0.374 mmol/L; P 〈 0.01 ）, respectively, together with the structural damages of glomerular atrophy and renal interstitial fibrosis. FGF21 treatment downregulated the ALP activity, calcium content in the kidney of VC rats by 42.1% （P 〈 0.01 ） and 11.7% （P 〈 0.05） as well as ameliorated the aortic injury and calcification as compared with VDN treatment alone group, indicating an ameliorative effect on VC. EL1SA assays showed that the expression of [3-Klotho, a component of FGF21 re

关键词： Chronic Fibroblast Growth Factor 21 Renal Insufficiency vascular calcification β-Klotho

Hydrogen sulfide ameliorates vascular calcification induced by vitamin D3 plus nicotine in rats

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Acta Pharmacologica Sinica 2006年第3期27卷 299-306页

作者： Sheng-ying WU~(2,6) Chun-shui PAN~3 Bin GENG~3 Jing ZHAO~3 Fang YU~3 Yong-zheng PANG~3 Chao-shu TANG~4 Yong-fen QI~(3,4,5) ~2Institute of Cardiovascular Disease,Peking University First Hospital.Beijing 100034 ~3Department of Physiology and Pathophysiology,Peking University Health Science Center,Beijing 100083,China,~4Key Laboratory of Molecular Cardiovascular Science,Ministry of Education,Beijing 100083,China Institute of Cardiovascular Disease Peking University First Hospital Beijing China Department of Physiology and Pathophysiology Peking University Health Science Center Beijing China Key Laboratory of Molecular Cardiovascular Science Ministry of Education Beijing China

Aim:To investigate the role of the endogenous cystathionine γ-synthase(CSE)/hydrogen sulfide(H2S)pathway in vascular calcification in vivo.Methods:A ratvascular calcification model was established by administration of vitamin D3 plusnicotine(VDN).The amount of CSE and osteopontin(OPN)mRNA was deter-mined by using semi-quantitative reverse-transcription polymerase chain reaction.The calcium content,45Ca2+accumulation and alkaline phosphatase(ALP)activitywere measured.H,S production and CSE activity were measured.Results:yonKossa staining produced strong positive black/brown staining in areas amongthe elastic fibers of the medial layer in the calcified aorta.The calcium content,45Ca2+accumulation and ALP activity in calcified arteries increased by 6.77-,1.42-,and 1.87-fold,respectively,compared with controls.The expression of the OPNgene was upregulated(Pvascularcalcification.H2S can ameliorate vascular calcification,suggesting that the H2S/CSE pathway plays a regulatory role in the pathogenesis of vascular calcification.

关键词： hydrogen sulfide cystathionine-lyase vascular calcification mRNA

Does treatment with statins have the potential of enhancing vascular calcification？

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Chinese Medical Journal 2008年第5期121卷 473-474页

作者： ZHANG Ming LI Xu-ping QIAO Yan NIE Shao-ping MA Chang-sheng Deparlanent of Cardiology Beijing Anzhen Hospital Capital Medical University Beijing 100029 China Department of Cardiology Second Xiangya Hospital Central South University Changsha Hunan 410011 China

vascular calcification is commonly found in atherosclerosis and recognized as a marker of atherosclerotic plaque burden. Many evdiences have demonstrated that vascular calcification is an active process and can be seen in all stages of development and intimately associated with atherosclerosis. The correlation between coronary calcifications and subclinical atherosclertotic disease has been well-known for some years. Bone morphogenetic protein-2 （BMP-2） has significant importance in bone development and the development of a wide array of tissues outside of bone. Zhang et al3,4 found mice genetically engineered to be deficient in BMP-2 die between days 7 and 10 of gestation of cardiac defects before bone formation. Many evidences have also confirmed that BMP-2 is a strong basic causative factor in vascular calcification and has been most frequently associated with calcific arteriopathy. Statins are the most powerful cholesterol-lowering drugs available. Although a major beneficial effect of statins in clinical studies is related to a marked reduction in low density lipoprotein （LDL） cholesterol levels, there are good evidences that statins hold multiple vascular protective effects,5 however, the effects of statins therapy in vascular calcification are more complex and less defined. The currently available reports of clinical trials about statins therapy of vascular calcification appeared to be paradoxical.

关键词： statins vascular calcification bone morphogenetic protein-2

Beneficial effect of berberine on atherosclerosis based on attenuating vascular inflammation and calcification

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中国药理学与毒理学杂志 2017年第10期31卷 993-994页

作者： Xiao-ming LI Qing-zhu WANG Lei GUO Institute of Basic Medical Sciences Chinese Academy of Medical SciencesDepartment of PharmacologSchool of Basic MedicinePeking Union Medical Colege

OBJECTIVE To investigate the beneficial effect of berberine(BBR)on atherosclerosisin Apo^(-/-) E mice and explore the underlying mechanisms based on attenuating vascular inflammation and modulating calcification in human umbilical vein endothelial cells(HUVECs) and smooth muscle cells(SMCs).METHODS 48 Apo-/-E mice,at 6-8 weeks old,were randomly allocated into 4 groups:normal,model,bbr and atorvastatin(positive control) groups with 12 mice in each group.They were fed with high-fat diet for 4 weeks except those in Normal group and then treated with indicated drugs orsolvent for another 4 weeks.The morphology and inflammation infiltration of aortic were examined with HE staining.The expression of BMP-2 in aortic was examined by immumohistochemical staining.Blood lipid levels were examined by automatic biochemical analyzer.The expression of IL-6,TNF-α and BMP-2 in serum and tissues was detected by ELISA method.The expression of ALP and the content of calcium were detected by commercially-available kits.HUVEC cells were stimulated with TNF-α and incubated with various concentrations of BBR for 24 h.The contents of intercellular cell adhesion molecule-1(ICAM-1),vascular cell adhesion molecule(VCAM-1),matrix metalloprotein-9(MMP-9) in the culture supernatant were detected by ELISA method.calcification was induced with β-glycerophosphatein SMC cells and the effect of BBR on the content of calcium was examined.RESULTS 4-week berberine treatment markedly lowered serum TC and LDL-c levels and improved the plaque stability in Apo-/-E mice fed with a high-fat diet(P<0.05 or P<0.01) which was comparable with the effect of atorvastatin.Berberineal so significantly decreased the levels of IL-6 and TNF-α in mice serum and aortic tissues(P<0.05 or P<0.001).Berberine tended to decrease ALP,BMP-2 levels and the content of calcium in mice serum and aortic tissues(P<0.05,P<0.01 or P<0.001) which were not observed in atorvastatin group.Berberine significantly lowered the levels of ICAM-1,VCAM-1,and MMP-9 in TNF-α-stimulated HUVECs.It c

关键词： berberine atherosclerosis vascular endothelium inflammation vascular calcification

Predictors of vascular calcification in Hemodialysis Patients

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Open Journal of Nephrology 2021年第2期11卷 273-280页

作者： Said Sayed Ahmed Khamis Ahmed Ragheb Tawfeek Mohammad Gamal Al Din Al-Helbawy Mohammad EL-Sayed Abdel Samea Heba Kamal Abd El Khalek Internal Medicine Department Faculty of Medicine Menoufia University Shibin El Kom Egypt Clinical Pathology Department Faculty of Medicine Menoufia University Shibin El Kom Egypt Diagnostic Medical and Interventional Radiology Department National Liver Institute Menoufia University Shibin El Kom Egypt

Background: The prevalence of both cardiovascular mortality and vascular calcification is much higher in patients with chronic kidney disease (CKD) than in the general population so early detection and intervention of VC may prevent or delay the progression and achieve improved patient outcomes. Objectives: To detect different predictors of vascular calcification in haemodialysis patients. Methods: This was a cross sectional observational study that included 85 patients with end stage renal disease (ESRD) on regular dialysis 47 males and 38 females ranged between 18 and 80 years old selected from Nephrology Unit, Internal Medicine Department, Menoufia University Hospital from April 2019 to May 2020. Serum calcium, phosphorus, alkhaline phosphatase, intact PTH, serum Matrix GLA protein, vitamin D and non-contrast CT for calcium scoring of femoral arteries were performed. Results: There was a significant correlation between age of the patient by years (p value 0.0001), serum calcium (p value 0.0001), phosphate (0.0001), calcium phosphate products (p value 0.0001) and alkhaline phosphatase (0.0001), and vascular calcification score detected by non-contrast CT on femoral arteries and negative correlation between serum Matrix GLA protein p value 0.0001) and the detected calcification score;the lower the MGP level the higher calcification score while there was no correlation between body mass index (BMI) (p value 0.021) intact PTH (p value 0.117), serum vitamin D level (p value 0.643), serum albumin (p value 0.643), serum haemoglobin (p value 0.257) and duration of dialysis (p value 0.260) and the detected score. Serum phosphate and calcium phosphorus product are independent risk factors for vascular calcification severity in haemodialysis patients. Conclusions: serum phosphate, calcium phosphate products are risk factors for vascular calcification while intact PTH vitamin D has no significant role in developing vascular calcification

关键词： vascular calcification Hemodialysis End Stage Renal Disease

The Pathogenesis of the Mechanism of FGF23 in Chronic Kidney Disease Patients with vascular calcification

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临床医学工程 2017年第S1期24卷 49-51页

作者： Shanshan LI Wenyu GNOG Sibo HUANG Lianghong YIN Bo HU Xiangnan DONG Taksui WONG Fanna LIU Yingyan LI Yueling ZHU Xin CHEN Baozhang GUAN Shengling HUANG Shuang CUI Bing YAN Hongwei HU Shaofeng HUANG Yongpin LU Shufei ZENG Chen YUN Berthold Hocher Wolfgang Pomme Department of Nephrology the First Affiliated Hospital of Jinan University Guangzhou Obers Medical Instrument Co. Ltd. Guangzhou Enttxs Medical Products Co. Ltd. Department of Nephrology Charité-Universitatsmediz in BerlinCampus Mitte University of Potsdam Institute of Nutritional Science KfH trustees for d Dialysis and Nierentransplantatione.v. Center of Neu-Isenburg

Fibroblast growth factor 23(FGF23)is a protein synthesized by bone cell and the osteoblast with endocrine function.The main role of FGF23 is to regulate serum phosphorus and 1,25(OH)2 D3 levels,it also plays an important role in calcium and phosphorus metabolism.The role of FGF23 in renal disease is to inhibit of phosphorus reabsorption,promote urinary phosphorus excretion and maintain a stable blood phosphorus level.Patients with chronic kidney disease(CKD)have more risk to suffer cardiovascular disease(CVD)which is related to the abnormal metabolism of calcium and phosphorus.FGF23,as newly discovered cardiovascular risk marker,several studies have shown that FGF23 level associates with multiple cardiovascular risk factors in CKD patients,especially in CKD patients with vascular calcification.To explore its pathogenesis of vascular calcification in CKD patients is particularly important,and that may help to take appropriate measures to improve the prognosis of CKD patients.

关键词： Fibroblast growth factor 23 Chronic kidney disease vascular calcification

A novel long-term intravenous combined with local treatment with human amnion-derived mesenchymal stem cells for a multidisciplinary rescued uremic calciphylaxis patient and the underlying mechanism

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Journal of Molecular Cell Biology 2022年第2期14卷 56-71页

作者： Lianju Qin Jing Zhang Yujie Xiao Kang Liu Yugui Cui Fangyan Xu Wenkai Ren Yanggang Yuan Chunyan Jiang Song Ning Xiaoxue Ye Ming Zeng Hanyang Qian Anning Bian Fan Li Guang Yang Shaowen Tang Zhihong Zhang Juncheng Dai Jing Guo Qiang Wang Bin Sun Yifei Ge Chun Ouyang Xueqiang Xu Jing Wang Yaoyu Huang Hongqing Cui Jing Zhou Meilian Wang Zhonglan Su Yan Lu Di Wu Jingping Shi Wei Liu Li Dong Yinbing Pan Baiqiao Zhao Ying Cui Xueyan Gao Zhanhui Gao Xiang Ma Aiqin Chen Jie Wang Meng Cao Qian Cui Li Chen Feng Chen Youjia Yu Qiang Ji Zhiwei Zhang Mufeng Gu Xiaojun Zhuang Xiaolin Lv Hui Wang Yanyan Pan Ling Wang Xianrong Xu Jing Zhao Xiuqin Wang Cuiping Liu Ningxia Liang Changying Xing Jiayin Liu Ningning Wang State Key Laboratory of Reproductive Medicine Center of Clinical Reproductive MedicineThe First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Nephrology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Epidemiology and Biostatistics School of Public HealthNanjing Medical UniversityNanjing 211166China Department of Pathology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Cardiology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Rheumatology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Obstetrics The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Dermatology The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Burn and Plastic Surgery The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Nuclear Medicine The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Infection The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Anesthesiology and Pain Management The First Affiliated Hospital of Nanjing Medical UniversityJiangsu Province HospitalNanjing 210029China Department of Nephrology The First People’s Hospital of LianyungangLianyungang 222061China Department of Nephrology Northern Jiangsu People’s HospitalYangzhou 225001China Department of General Medicine Geriatric Hospital of Nanjing Medical UniversityNanjing 210024China Department of Nephrology BenQ Medical CenterThe Affiliated BenQ Hospital of Nanjing Medical Uni

Calciphylaxis is a rare disease characterized histologically by microvessel calcification and microthrombosis,with high mortality and no proven therapy.Here,we reported a severe uremic calciphylaxis patient with progressive skin ischemia,large areas of painful malodorous ulcers,and mummified legs.Because of the worsening symptoms and signs refractory to conventional therapies,treatment with human amnion-derived mesenchymal stem cells(hAMSCs)was approved.Preclinical release inspections of hAMSCs,efficacy,and safety assessment,including cytokine secretory ability,immunocompetence,tumorigenicity,and genetics analysis in vitro,were introduced.We further performed acute and long-term hAMSC toxicity evaluations in C57BL/6 mice and rats,abnormal immune response tests in C57BL/6 mice,and tumorigenicity tests in neonatal Balbc-nu nude mice.After the preclinical research,the patient was treated with hAMSCs by intravenous and local intramuscular injection and external supernatant application to the ulcers.When followed up to 15 months,the blood-based markers of bone and mineral metabolism improved,with skin soft tissue regeneration and a more favorable profile of peripheral blood mononuclear cells.Skin biopsy after 1-month treatment showed vascular regeneration with mature noncalcified vessels within the dermis,and 20 months later,the re-epithelialization restored the integrity of the damaged site.No infusion or local treatment-related adverse events occurred.Thus,this novel long-term intravenous combined with local treatment with hAMSCs warrants further investigation as a potential regenerative treatment for uremic calciphylaxis due to effects of inhibiting vascular calcification,stimulating angiogenesis and myogenesis,anti-inflammatory and immune modulation,multidifferentiation,re-epithelialization,and restoration of integrity.

关键词： calciphylaxis chronic kidney disease vascular calcification multidisciplinary rescue human amnion-derived mesenchymal stem cells preclinical research regenerative medicine