CML/RAGE signal induces calcification cascade in diabetes
Vascular calcification is a significant predictor of coronary heart disease events, stroke, and lower-limb amputation. Advanced glycation end-products (AGEs) play a key role in the development of vascular calcification. However, the role of Nε-carboxymethyl-lysine (CML), a major active ingredient of...
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| description | Vascular calcification is a significant predictor of coronary heart disease events, stroke, and lower-limb amputation. Advanced glycation end-products (AGEs) play a key role in the development of vascular calcification. However, the role of Nε-carboxymethyl-lysine (CML), a major active ingredient of heterogeneous AGEs, in the development of atherosclerotic calcification in diabetic patients and the underlying mechanism remain unclear. Hence, the role and the mechanism of CML in the transmission pathway of diabetic calcification cascade were investigated in the present study.
In vivo and in vitro investigations were performed. In study I, 45 diabetic patients hospitalized for above-knee amputation in the Department of Orthopedics, Affiliated Hospital of Jiangsu University were recruited from February 2010 to June 2015. The patients were categorized based on the severity of anterior tibial artery stenosis, which was assessed by color Doppler ultrasound, into mild stenosis (0% |
| doi_str_mv | 10.1186/s13098-016-0196-7 |
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| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5192585</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A475343497</galeid><sourcerecordid>A475343497</sourcerecordid><originalsourceid>FETCH-LOGICAL-c525t-592ea55d39087af268518a6d6d27f7e0645899d26c611d1b138d2684c207f5f33</originalsourceid><addsrcrecordid>eNptkktrGzEUhUVJiNMkP6CbYCiUbibRY_TaFIxxnYJLoTRrIethy8ijZDQTyL-vpnYTO2QhpCt991w4OgB8QvAGIcFuMyJQigoiVpZkFf8AzhGnoqJSspOD8wh8zHkDIeOU12dghAUkFNfkHMjpz8Xt78l8Ns5h1eg4Do3tjctjo6MJPhjdhdSUKhttXXkd26CXrnP5Epx6HbO72u8X4P777M_0rlr8mv-YThaVoZh2ZTx2mlJLJBRce8wERUIzyyzmnjvIaiqktJgZhpBFS0REKURtMOSeekIuwLed7kO_3DprXNO1OqqHNmx1-6ySDur4pQlrtUpPiiKJqaBF4OteoE2Pvcud2oZsXIy6canPCglas2IVQQX9_AbdpL4ttvyjKCRMMvhKrXR0KjQ-lblmEFWTuujUpJa8UDfvUHqwcRtMapwP5f6o4ctBw9rp2K1ziv3wAfkYRDvQtCnn1vkXMxBUQzDULhiqBEMNwVBDz_Whiy8d_5NA_gIaea72</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1855036960</pqid></control><display><type>article</type><title>CML/RAGE signal induces calcification cascade in diabetes</title><source>DOAJ Directory of Open Access Journals</source><source>PubMed Central Open Access</source><source>Springer Nature OA Free Journals</source><source>EZB-FREE-00999 freely available EZB journals</source><source>PubMed Central</source><source>SpringerLink Journals - AutoHoldings</source><creator>Wang, Zhongqun ; Li, Lihua ; Du, Rui ; Yan, Jinchuan ; Liu, Naifeng ; Yuan, Wei ; Jiang, Yicheng ; Xu, Suining ; Ye, Fei ; Yuan, Guoyue ; Zhang, Baohai ; Liu, Peijing</creator><creatorcontrib>Wang, Zhongqun ; Li, Lihua ; Du, Rui ; Yan, Jinchuan ; Liu, Naifeng ; Yuan, Wei ; Jiang, Yicheng ; Xu, Suining ; Ye, Fei ; Yuan, Guoyue ; Zhang, Baohai ; Liu, Peijing</creatorcontrib><description>Vascular calcification is a significant predictor of coronary heart disease events, stroke, and lower-limb amputation. Advanced glycation end-products (AGEs) play a key role in the development of vascular calcification. However, the role of Nε-carboxymethyl-lysine (CML), a major active ingredient of heterogeneous AGEs, in the development of atherosclerotic calcification in diabetic patients and the underlying mechanism remain unclear. Hence, the role and the mechanism of CML in the transmission pathway of diabetic calcification cascade were investigated in the present study.
In vivo and in vitro investigations were performed. In study I, 45 diabetic patients hospitalized for above-knee amputation in the Department of Orthopedics, Affiliated Hospital of Jiangsu University were recruited from February 2010 to June 2015. The patients were categorized based on the severity of anterior tibial artery stenosis, which was assessed by color Doppler ultrasound, into mild stenosis (0% < stenosis < 50%, n = 15), moderate stenosis (50 ≤ stenosis < 70%, n = 15), and severe stenosis/occlusion groups (70 ≤ stenosis ≤ 100%, n = 15). In study II, the specific mechanism of CML in the transmission pathway of the diabetic calcification cascade signal was investigated in A7r5 aortic smooth muscle cells under high-lipid, apoptosis-coexisting conditions. ELISA (for serum CML concentration of patients), ultrasound (for plaque size, calcification, blood flow filling, vascular stenosis etc.), H&E staining (for plaque morphology), vonKossa staining (for qualitative analysis of calcification), calcium content assay (for quantitative analysis of calcification), and Western blot analyses of CML, receptor for advanced glycation end products (RAGE), NADPH oxidase 4, phosphorylated p38, core-binding factor α1 (cbfα1), alkaline phosphatase (ALP) and β-actin were then performed.
Morphological analysis revealed extensive calcification lesions in the intima and media of the anterior tibial artery. The extent and area of calcium deposition in the intima significantly increased with disease progression. Interestingly, spotty calcification was predominant in the atherosclerotic plaques of diabetic patients with amputation, and macrocalcification was almost invisible. Pearson correlation analysis revealed that serum CML level exhibited a significant positive correlation with calcium content in the arterial wall (R
= 0.6141,
< 0.0001). Semi-quantitative Western blot analysis suggested that the intensity of CML/RAGE signal increased with progression of atherosclerotic calcification in diabetic patients. In subsequent in vitro study, the related pathway was blocked by anti-RAGE antibody, NADPH oxidase inhibitor DPI, p38MAPK inhibitor SB203580, and anti-cbfa1 antibody in a step-wise manner to observe changes in calcium deposition and molecular signals. Results suggested that CML may play a key role in atherosclerotic calcification mainly through the CML/RAGE- reactive oxygen species (ROS)-p38MAPK-cbfα1-ALP pathway.
Spotty calcification was predominant in the atherosclerotic plaques of amputated diabetic patients. CML/RAGE signal may induce the calcification cascade in diabetes via ROS-p38MAPK.</description><identifier>ISSN: 1758-5996</identifier><identifier>EISSN: 1758-5996</identifier><identifier>DOI: 10.1186/s13098-016-0196-7</identifier><identifier>PMID: 28035243</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Advanced glycation end products ; Atherosclerosis ; Complications and side effects ; Coronary heart disease ; Diabetes mellitus ; Genetic aspects ; Risk factors</subject><ispartof>Diabetology and metabolic syndrome, 2016-12, Vol.8 (1), p.83-83, Article 83</ispartof><rights>COPYRIGHT 2016 BioMed Central Ltd.</rights><rights>Copyright BioMed Central 2016</rights><rights>The Author(s) 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-592ea55d39087af268518a6d6d27f7e0645899d26c611d1b138d2684c207f5f33</citedby><cites>FETCH-LOGICAL-c525t-592ea55d39087af268518a6d6d27f7e0645899d26c611d1b138d2684c207f5f33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5192585/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5192585/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,27905,27906,53772,53774</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28035243$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Zhongqun</creatorcontrib><creatorcontrib>Li, Lihua</creatorcontrib><creatorcontrib>Du, Rui</creatorcontrib><creatorcontrib>Yan, Jinchuan</creatorcontrib><creatorcontrib>Liu, Naifeng</creatorcontrib><creatorcontrib>Yuan, Wei</creatorcontrib><creatorcontrib>Jiang, Yicheng</creatorcontrib><creatorcontrib>Xu, Suining</creatorcontrib><creatorcontrib>Ye, Fei</creatorcontrib><creatorcontrib>Yuan, Guoyue</creatorcontrib><creatorcontrib>Zhang, Baohai</creatorcontrib><creatorcontrib>Liu, Peijing</creatorcontrib><title>CML/RAGE signal induces calcification cascade in diabetes</title><title>Diabetology and metabolic syndrome</title><addtitle>Diabetol Metab Syndr</addtitle><description>Vascular calcification is a significant predictor of coronary heart disease events, stroke, and lower-limb amputation. Advanced glycation end-products (AGEs) play a key role in the development of vascular calcification. However, the role of Nε-carboxymethyl-lysine (CML), a major active ingredient of heterogeneous AGEs, in the development of atherosclerotic calcification in diabetic patients and the underlying mechanism remain unclear. Hence, the role and the mechanism of CML in the transmission pathway of diabetic calcification cascade were investigated in the present study.
In vivo and in vitro investigations were performed. In study I, 45 diabetic patients hospitalized for above-knee amputation in the Department of Orthopedics, Affiliated Hospital of Jiangsu University were recruited from February 2010 to June 2015. The patients were categorized based on the severity of anterior tibial artery stenosis, which was assessed by color Doppler ultrasound, into mild stenosis (0% < stenosis < 50%, n = 15), moderate stenosis (50 ≤ stenosis < 70%, n = 15), and severe stenosis/occlusion groups (70 ≤ stenosis ≤ 100%, n = 15). In study II, the specific mechanism of CML in the transmission pathway of the diabetic calcification cascade signal was investigated in A7r5 aortic smooth muscle cells under high-lipid, apoptosis-coexisting conditions. ELISA (for serum CML concentration of patients), ultrasound (for plaque size, calcification, blood flow filling, vascular stenosis etc.), H&E staining (for plaque morphology), vonKossa staining (for qualitative analysis of calcification), calcium content assay (for quantitative analysis of calcification), and Western blot analyses of CML, receptor for advanced glycation end products (RAGE), NADPH oxidase 4, phosphorylated p38, core-binding factor α1 (cbfα1), alkaline phosphatase (ALP) and β-actin were then performed.
Morphological analysis revealed extensive calcification lesions in the intima and media of the anterior tibial artery. The extent and area of calcium deposition in the intima significantly increased with disease progression. Interestingly, spotty calcification was predominant in the atherosclerotic plaques of diabetic patients with amputation, and macrocalcification was almost invisible. Pearson correlation analysis revealed that serum CML level exhibited a significant positive correlation with calcium content in the arterial wall (R
= 0.6141,
< 0.0001). Semi-quantitative Western blot analysis suggested that the intensity of CML/RAGE signal increased with progression of atherosclerotic calcification in diabetic patients. In subsequent in vitro study, the related pathway was blocked by anti-RAGE antibody, NADPH oxidase inhibitor DPI, p38MAPK inhibitor SB203580, and anti-cbfa1 antibody in a step-wise manner to observe changes in calcium deposition and molecular signals. Results suggested that CML may play a key role in atherosclerotic calcification mainly through the CML/RAGE- reactive oxygen species (ROS)-p38MAPK-cbfα1-ALP pathway.
Spotty calcification was predominant in the atherosclerotic plaques of amputated diabetic patients. CML/RAGE signal may induce the calcification cascade in diabetes via ROS-p38MAPK.</description><subject>Advanced glycation end products</subject><subject>Atherosclerosis</subject><subject>Complications and side effects</subject><subject>Coronary heart disease</subject><subject>Diabetes mellitus</subject><subject>Genetic aspects</subject><subject>Risk factors</subject><issn>1758-5996</issn><issn>1758-5996</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><recordid>eNptkktrGzEUhUVJiNMkP6CbYCiUbibRY_TaFIxxnYJLoTRrIethy8ijZDQTyL-vpnYTO2QhpCt991w4OgB8QvAGIcFuMyJQigoiVpZkFf8AzhGnoqJSspOD8wh8zHkDIeOU12dghAUkFNfkHMjpz8Xt78l8Ns5h1eg4Do3tjctjo6MJPhjdhdSUKhttXXkd26CXrnP5Epx6HbO72u8X4P777M_0rlr8mv-YThaVoZh2ZTx2mlJLJBRce8wERUIzyyzmnjvIaiqktJgZhpBFS0REKURtMOSeekIuwLed7kO_3DprXNO1OqqHNmx1-6ySDur4pQlrtUpPiiKJqaBF4OteoE2Pvcud2oZsXIy6canPCglas2IVQQX9_AbdpL4ttvyjKCRMMvhKrXR0KjQ-lblmEFWTuujUpJa8UDfvUHqwcRtMapwP5f6o4ctBw9rp2K1ziv3wAfkYRDvQtCnn1vkXMxBUQzDULhiqBEMNwVBDz_Whiy8d_5NA_gIaea72</recordid><startdate>20161228</startdate><enddate>20161228</enddate><creator>Wang, Zhongqun</creator><creator>Li, Lihua</creator><creator>Du, Rui</creator><creator>Yan, Jinchuan</creator><creator>Liu, Naifeng</creator><creator>Yuan, Wei</creator><creator>Jiang, Yicheng</creator><creator>Xu, Suining</creator><creator>Ye, Fei</creator><creator>Yuan, Guoyue</creator><creator>Zhang, Baohai</creator><creator>Liu, Peijing</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7TS</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20161228</creationdate><title>CML/RAGE signal induces calcification cascade in diabetes</title><author>Wang, Zhongqun ; Li, Lihua ; Du, Rui ; Yan, Jinchuan ; Liu, Naifeng ; Yuan, Wei ; Jiang, Yicheng ; Xu, Suining ; Ye, Fei ; Yuan, Guoyue ; Zhang, Baohai ; Liu, Peijing</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-592ea55d39087af268518a6d6d27f7e0645899d26c611d1b138d2684c207f5f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Advanced glycation end products</topic><topic>Atherosclerosis</topic><topic>Complications and side effects</topic><topic>Coronary heart disease</topic><topic>Diabetes mellitus</topic><topic>Genetic aspects</topic><topic>Risk factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Zhongqun</creatorcontrib><creatorcontrib>Li, Lihua</creatorcontrib><creatorcontrib>Du, Rui</creatorcontrib><creatorcontrib>Yan, Jinchuan</creatorcontrib><creatorcontrib>Liu, Naifeng</creatorcontrib><creatorcontrib>Yuan, Wei</creatorcontrib><creatorcontrib>Jiang, Yicheng</creatorcontrib><creatorcontrib>Xu, Suining</creatorcontrib><creatorcontrib>Ye, Fei</creatorcontrib><creatorcontrib>Yuan, Guoyue</creatorcontrib><creatorcontrib>Zhang, Baohai</creatorcontrib><creatorcontrib>Liu, Peijing</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetology and metabolic syndrome</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Zhongqun</au><au>Li, Lihua</au><au>Du, Rui</au><au>Yan, Jinchuan</au><au>Liu, Naifeng</au><au>Yuan, Wei</au><au>Jiang, Yicheng</au><au>Xu, Suining</au><au>Ye, Fei</au><au>Yuan, Guoyue</au><au>Zhang, Baohai</au><au>Liu, Peijing</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CML/RAGE signal induces calcification cascade in diabetes</atitle><jtitle>Diabetology and metabolic syndrome</jtitle><addtitle>Diabetol Metab Syndr</addtitle><date>2016-12-28</date><risdate>2016</risdate><volume>8</volume><issue>1</issue><spage>83</spage><epage>83</epage><pages>83-83</pages><artnum>83</artnum><issn>1758-5996</issn><eissn>1758-5996</eissn><abstract>Vascular calcification is a significant predictor of coronary heart disease events, stroke, and lower-limb amputation. Advanced glycation end-products (AGEs) play a key role in the development of vascular calcification. However, the role of Nε-carboxymethyl-lysine (CML), a major active ingredient of heterogeneous AGEs, in the development of atherosclerotic calcification in diabetic patients and the underlying mechanism remain unclear. Hence, the role and the mechanism of CML in the transmission pathway of diabetic calcification cascade were investigated in the present study.
In vivo and in vitro investigations were performed. In study I, 45 diabetic patients hospitalized for above-knee amputation in the Department of Orthopedics, Affiliated Hospital of Jiangsu University were recruited from February 2010 to June 2015. The patients were categorized based on the severity of anterior tibial artery stenosis, which was assessed by color Doppler ultrasound, into mild stenosis (0% < stenosis < 50%, n = 15), moderate stenosis (50 ≤ stenosis < 70%, n = 15), and severe stenosis/occlusion groups (70 ≤ stenosis ≤ 100%, n = 15). In study II, the specific mechanism of CML in the transmission pathway of the diabetic calcification cascade signal was investigated in A7r5 aortic smooth muscle cells under high-lipid, apoptosis-coexisting conditions. ELISA (for serum CML concentration of patients), ultrasound (for plaque size, calcification, blood flow filling, vascular stenosis etc.), H&E staining (for plaque morphology), vonKossa staining (for qualitative analysis of calcification), calcium content assay (for quantitative analysis of calcification), and Western blot analyses of CML, receptor for advanced glycation end products (RAGE), NADPH oxidase 4, phosphorylated p38, core-binding factor α1 (cbfα1), alkaline phosphatase (ALP) and β-actin were then performed.
Morphological analysis revealed extensive calcification lesions in the intima and media of the anterior tibial artery. The extent and area of calcium deposition in the intima significantly increased with disease progression. Interestingly, spotty calcification was predominant in the atherosclerotic plaques of diabetic patients with amputation, and macrocalcification was almost invisible. Pearson correlation analysis revealed that serum CML level exhibited a significant positive correlation with calcium content in the arterial wall (R
= 0.6141,
< 0.0001). Semi-quantitative Western blot analysis suggested that the intensity of CML/RAGE signal increased with progression of atherosclerotic calcification in diabetic patients. In subsequent in vitro study, the related pathway was blocked by anti-RAGE antibody, NADPH oxidase inhibitor DPI, p38MAPK inhibitor SB203580, and anti-cbfa1 antibody in a step-wise manner to observe changes in calcium deposition and molecular signals. Results suggested that CML may play a key role in atherosclerotic calcification mainly through the CML/RAGE- reactive oxygen species (ROS)-p38MAPK-cbfα1-ALP pathway.
Spotty calcification was predominant in the atherosclerotic plaques of amputated diabetic patients. CML/RAGE signal may induce the calcification cascade in diabetes via ROS-p38MAPK.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>28035243</pmid><doi>10.1186/s13098-016-0196-7</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| source | DOAJ Directory of Open Access Journals; PubMed Central Open Access; Springer Nature OA Free Journals; EZB-FREE-00999 freely available EZB journals; PubMed Central; SpringerLink Journals - AutoHoldings |
| subjects | Advanced glycation end products Atherosclerosis Complications and side effects Coronary heart disease Diabetes mellitus Genetic aspects Risk factors |
| title | CML/RAGE signal induces calcification cascade in diabetes |
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