Proteomic and metabolomic characterization of streptozotocin-induced diabetic nephropathy in TIMP3-deficient mice
Aims The tissue inhibitor of metalloproteinase TIMP3 is a stromal protein that restrains the activity of both protease and receptor in the extracellular matrix and has been found to be down-regulated in diabetic nephropathy (DN), the leading cause of end-stage renal disease in developed countries. M...
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| Veröffentlicht in: | Acta diabetologica 2018-02, Vol.55 (2), p.121-129 |
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| creator | Rossi, Claudia Marzano, Valeria Consalvo, Ada Zucchelli, Mirco Levi Mortera, Stefano Casagrande, Viviana Mavilio, Maria Sacchetta, Paolo Federici, Massimo Menghini, Rossella Urbani, Andrea Ciavardelli, Domenico |
| description | Aims
The tissue inhibitor of metalloproteinase TIMP3 is a stromal protein that restrains the activity of both protease and receptor in the extracellular matrix and has been found to be down-regulated in diabetic nephropathy (DN), the leading cause of end-stage renal disease in developed countries.
Methods
In order to gain deeper insights on the association of loss of TIMP3 and DN, we performed differential proteomic analysis of kidney and blood metabolic profiling of wild-type and Timp3-knockout mice before and after streptozotocin (STZ) treatment, widely used to induce insulin deficiency and hyperglycemia.
Results
Kidney proteomic data and blood metabolic profiles suggest significant alterations of peroxisomal and mitochondrial fatty acids β-oxidation in Timp3-knockout mice compared to wild-type mice under basal condition. These alterations were exacerbated in response to STZ treatment.
Conclusions
Proteomic and metabolomic approaches showed that loss of TIMP3 alone or in combination with STZ treatment results in significant alterations of kidney lipid metabolism and peripheral acylcarnitine levels, supporting the idea that loss of TIMP3 may generate a phenotype more prone to DN. |
| doi_str_mv | 10.1007/s00592-017-1074-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1964270390</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1963300803</sourcerecordid><originalsourceid>FETCH-LOGICAL-c372t-fd841a09fad86899c5df770ca05b1a72e3deac8970b203e7994367d4da5fba663</originalsourceid><addsrcrecordid>eNp1kcFu1DAQhi1ERZfCA3BBkbhwMR3bSRwfUVWgUlF7KGfLsSesq42d2s5h-_R4uwUhJE7WyN__z0gfIe8YfGIA8jwDdIpTYJIykC3dvyAb1gpOOy7ES7IB1QLtWq5Oyeuc7wEYl2J4RU65YqLlQ78hD7cpFoyzt40JrpmxmDHunma7NcnYgsk_muJjaOLU5JJwKfExlmh9oD641aJrnDcjlpoJuGxTXEzZ7hsfmrur77eCOpy89RhKU2vxDTmZzC7j2-f3jPz4cnl38Y1e33y9uvh8Ta2QvNDJDS0zoCbjhn5QynZukhKsgW5kRnIUDo0dlISRg0CpVCt66Vpnumk0fS_OyMdj75Liw4q56Nlni7udCRjXrJnqWy5BKKjoh3_Q-7imUK87UEIADCAqxY6UTTHnhJNekp9N2msG-uBDH33o6kMffOh9zbx_bl7HGd2fxG8BFeBHINev8BPTX6v_2_oL5P6X1A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1963300803</pqid></control><display><type>article</type><title>Proteomic and metabolomic characterization of streptozotocin-induced diabetic nephropathy in TIMP3-deficient mice</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Rossi, Claudia ; Marzano, Valeria ; Consalvo, Ada ; Zucchelli, Mirco ; Levi Mortera, Stefano ; Casagrande, Viviana ; Mavilio, Maria ; Sacchetta, Paolo ; Federici, Massimo ; Menghini, Rossella ; Urbani, Andrea ; Ciavardelli, Domenico</creator><creatorcontrib>Rossi, Claudia ; Marzano, Valeria ; Consalvo, Ada ; Zucchelli, Mirco ; Levi Mortera, Stefano ; Casagrande, Viviana ; Mavilio, Maria ; Sacchetta, Paolo ; Federici, Massimo ; Menghini, Rossella ; Urbani, Andrea ; Ciavardelli, Domenico</creatorcontrib><description>Aims
The tissue inhibitor of metalloproteinase TIMP3 is a stromal protein that restrains the activity of both protease and receptor in the extracellular matrix and has been found to be down-regulated in diabetic nephropathy (DN), the leading cause of end-stage renal disease in developed countries.
Methods
In order to gain deeper insights on the association of loss of TIMP3 and DN, we performed differential proteomic analysis of kidney and blood metabolic profiling of wild-type and Timp3-knockout mice before and after streptozotocin (STZ) treatment, widely used to induce insulin deficiency and hyperglycemia.
Results
Kidney proteomic data and blood metabolic profiles suggest significant alterations of peroxisomal and mitochondrial fatty acids β-oxidation in Timp3-knockout mice compared to wild-type mice under basal condition. These alterations were exacerbated in response to STZ treatment.
Conclusions
Proteomic and metabolomic approaches showed that loss of TIMP3 alone or in combination with STZ treatment results in significant alterations of kidney lipid metabolism and peripheral acylcarnitine levels, supporting the idea that loss of TIMP3 may generate a phenotype more prone to DN.</description><identifier>ISSN: 0940-5429</identifier><identifier>EISSN: 1432-5233</identifier><identifier>DOI: 10.1007/s00592-017-1074-y</identifier><identifier>PMID: 29134286</identifier><language>eng</language><publisher>Milan: Springer Milan</publisher><subject>Animals ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental - chemically induced ; Diabetes Mellitus, Experimental - complications ; Diabetes Mellitus, Experimental - metabolism ; Diabetic Nephropathies - chemically induced ; Diabetic Nephropathies - genetics ; Diabetic Nephropathies - metabolism ; Diabetic Nephropathies - pathology ; Diabetic nephropathy ; End-stage renal disease ; Extracellular matrix ; Fatty acids ; Hyperglycemia ; Insulin ; Internal Medicine ; Kidney - metabolism ; Kidney diseases ; Kidney Failure, Chronic - chemically induced ; Kidney Failure, Chronic - genetics ; Kidney Failure, Chronic - metabolism ; Kidney Failure, Chronic - pathology ; Lipid Metabolism ; Medicine ; Medicine & Public Health ; Metabolic Diseases ; Metabolism ; Metabolome ; Metabolomics ; Metalloproteinase ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitochondria ; Nephropathy ; Original Article ; Oxidation ; Proteome - analysis ; Proteome - metabolism ; Proteomics ; Rodents ; Streptozocin ; Tissue inhibitor of metalloproteinase 3 ; Tissue Inhibitor of Metalloproteinase-3 - genetics</subject><ispartof>Acta diabetologica, 2018-02, Vol.55 (2), p.121-129</ispartof><rights>Springer-Verlag Italia S.r.l., part of Springer Nature 2017</rights><rights>Acta Diabetologica is a copyright of Springer, (2017). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c372t-fd841a09fad86899c5df770ca05b1a72e3deac8970b203e7994367d4da5fba663</citedby><cites>FETCH-LOGICAL-c372t-fd841a09fad86899c5df770ca05b1a72e3deac8970b203e7994367d4da5fba663</cites><orcidid>0000-0003-0949-0280 ; 0000-0002-1410-3946 ; 0000-0003-4989-5194 ; 0000-0002-1087-847X ; 0000-0001-6184-0933 ; 0000-0001-8397-2355 ; 0000-0001-9168-3174 ; 0000-0003-3860-9404 ; 0000-0001-6364-2121</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00592-017-1074-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00592-017-1074-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27924,27925,41488,42557,51319</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29134286$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Rossi, Claudia</creatorcontrib><creatorcontrib>Marzano, Valeria</creatorcontrib><creatorcontrib>Consalvo, Ada</creatorcontrib><creatorcontrib>Zucchelli, Mirco</creatorcontrib><creatorcontrib>Levi Mortera, Stefano</creatorcontrib><creatorcontrib>Casagrande, Viviana</creatorcontrib><creatorcontrib>Mavilio, Maria</creatorcontrib><creatorcontrib>Sacchetta, Paolo</creatorcontrib><creatorcontrib>Federici, Massimo</creatorcontrib><creatorcontrib>Menghini, Rossella</creatorcontrib><creatorcontrib>Urbani, Andrea</creatorcontrib><creatorcontrib>Ciavardelli, Domenico</creatorcontrib><title>Proteomic and metabolomic characterization of streptozotocin-induced diabetic nephropathy in TIMP3-deficient mice</title><title>Acta diabetologica</title><addtitle>Acta Diabetol</addtitle><addtitle>Acta Diabetol</addtitle><description>Aims
The tissue inhibitor of metalloproteinase TIMP3 is a stromal protein that restrains the activity of both protease and receptor in the extracellular matrix and has been found to be down-regulated in diabetic nephropathy (DN), the leading cause of end-stage renal disease in developed countries.
Methods
In order to gain deeper insights on the association of loss of TIMP3 and DN, we performed differential proteomic analysis of kidney and blood metabolic profiling of wild-type and Timp3-knockout mice before and after streptozotocin (STZ) treatment, widely used to induce insulin deficiency and hyperglycemia.
Results
Kidney proteomic data and blood metabolic profiles suggest significant alterations of peroxisomal and mitochondrial fatty acids β-oxidation in Timp3-knockout mice compared to wild-type mice under basal condition. These alterations were exacerbated in response to STZ treatment.
Conclusions
Proteomic and metabolomic approaches showed that loss of TIMP3 alone or in combination with STZ treatment results in significant alterations of kidney lipid metabolism and peripheral acylcarnitine levels, supporting the idea that loss of TIMP3 may generate a phenotype more prone to DN.</description><subject>Animals</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental - chemically induced</subject><subject>Diabetes Mellitus, Experimental - complications</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetic Nephropathies - chemically induced</subject><subject>Diabetic Nephropathies - genetics</subject><subject>Diabetic Nephropathies - metabolism</subject><subject>Diabetic Nephropathies - pathology</subject><subject>Diabetic nephropathy</subject><subject>End-stage renal disease</subject><subject>Extracellular matrix</subject><subject>Fatty acids</subject><subject>Hyperglycemia</subject><subject>Insulin</subject><subject>Internal Medicine</subject><subject>Kidney - metabolism</subject><subject>Kidney diseases</subject><subject>Kidney Failure, Chronic - chemically induced</subject><subject>Kidney Failure, Chronic - genetics</subject><subject>Kidney Failure, Chronic - metabolism</subject><subject>Kidney Failure, Chronic - pathology</subject><subject>Lipid Metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolic Diseases</subject><subject>Metabolism</subject><subject>Metabolome</subject><subject>Metabolomics</subject><subject>Metalloproteinase</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mitochondria</subject><subject>Nephropathy</subject><subject>Original Article</subject><subject>Oxidation</subject><subject>Proteome - analysis</subject><subject>Proteome - metabolism</subject><subject>Proteomics</subject><subject>Rodents</subject><subject>Streptozocin</subject><subject>Tissue inhibitor of metalloproteinase 3</subject><subject>Tissue Inhibitor of Metalloproteinase-3 - genetics</subject><issn>0940-5429</issn><issn>1432-5233</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNp1kcFu1DAQhi1ERZfCA3BBkbhwMR3bSRwfUVWgUlF7KGfLsSesq42d2s5h-_R4uwUhJE7WyN__z0gfIe8YfGIA8jwDdIpTYJIykC3dvyAb1gpOOy7ES7IB1QLtWq5Oyeuc7wEYl2J4RU65YqLlQ78hD7cpFoyzt40JrpmxmDHunma7NcnYgsk_muJjaOLU5JJwKfExlmh9oD641aJrnDcjlpoJuGxTXEzZ7hsfmrur77eCOpy89RhKU2vxDTmZzC7j2-f3jPz4cnl38Y1e33y9uvh8Ta2QvNDJDS0zoCbjhn5QynZukhKsgW5kRnIUDo0dlISRg0CpVCt66Vpnumk0fS_OyMdj75Liw4q56Nlni7udCRjXrJnqWy5BKKjoh3_Q-7imUK87UEIADCAqxY6UTTHnhJNekp9N2msG-uBDH33o6kMffOh9zbx_bl7HGd2fxG8BFeBHINev8BPTX6v_2_oL5P6X1A</recordid><startdate>20180201</startdate><enddate>20180201</enddate><creator>Rossi, Claudia</creator><creator>Marzano, Valeria</creator><creator>Consalvo, Ada</creator><creator>Zucchelli, Mirco</creator><creator>Levi Mortera, Stefano</creator><creator>Casagrande, Viviana</creator><creator>Mavilio, Maria</creator><creator>Sacchetta, Paolo</creator><creator>Federici, Massimo</creator><creator>Menghini, Rossella</creator><creator>Urbani, Andrea</creator><creator>Ciavardelli, Domenico</creator><general>Springer Milan</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</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>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-0949-0280</orcidid><orcidid>https://orcid.org/0000-0002-1410-3946</orcidid><orcidid>https://orcid.org/0000-0003-4989-5194</orcidid><orcidid>https://orcid.org/0000-0002-1087-847X</orcidid><orcidid>https://orcid.org/0000-0001-6184-0933</orcidid><orcidid>https://orcid.org/0000-0001-8397-2355</orcidid><orcidid>https://orcid.org/0000-0001-9168-3174</orcidid><orcidid>https://orcid.org/0000-0003-3860-9404</orcidid><orcidid>https://orcid.org/0000-0001-6364-2121</orcidid></search><sort><creationdate>20180201</creationdate><title>Proteomic and metabolomic characterization of streptozotocin-induced diabetic nephropathy in TIMP3-deficient mice</title><author>Rossi, Claudia ; Marzano, Valeria ; Consalvo, Ada ; Zucchelli, Mirco ; Levi Mortera, Stefano ; Casagrande, Viviana ; Mavilio, Maria ; Sacchetta, Paolo ; Federici, Massimo ; Menghini, Rossella ; Urbani, Andrea ; Ciavardelli, Domenico</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c372t-fd841a09fad86899c5df770ca05b1a72e3deac8970b203e7994367d4da5fba663</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental - chemically induced</topic><topic>Diabetes Mellitus, Experimental - complications</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetic Nephropathies - chemically induced</topic><topic>Diabetic Nephropathies - genetics</topic><topic>Diabetic Nephropathies - metabolism</topic><topic>Diabetic Nephropathies - pathology</topic><topic>Diabetic nephropathy</topic><topic>End-stage renal disease</topic><topic>Extracellular matrix</topic><topic>Fatty acids</topic><topic>Hyperglycemia</topic><topic>Insulin</topic><topic>Internal Medicine</topic><topic>Kidney - metabolism</topic><topic>Kidney diseases</topic><topic>Kidney Failure, Chronic - chemically induced</topic><topic>Kidney Failure, Chronic - genetics</topic><topic>Kidney Failure, Chronic - metabolism</topic><topic>Kidney Failure, Chronic - pathology</topic><topic>Lipid Metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolic Diseases</topic><topic>Metabolism</topic><topic>Metabolome</topic><topic>Metabolomics</topic><topic>Metalloproteinase</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Mitochondria</topic><topic>Nephropathy</topic><topic>Original Article</topic><topic>Oxidation</topic><topic>Proteome - analysis</topic><topic>Proteome - metabolism</topic><topic>Proteomics</topic><topic>Rodents</topic><topic>Streptozocin</topic><topic>Tissue inhibitor of metalloproteinase 3</topic><topic>Tissue Inhibitor of Metalloproteinase-3 - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Rossi, Claudia</creatorcontrib><creatorcontrib>Marzano, Valeria</creatorcontrib><creatorcontrib>Consalvo, Ada</creatorcontrib><creatorcontrib>Zucchelli, Mirco</creatorcontrib><creatorcontrib>Levi Mortera, Stefano</creatorcontrib><creatorcontrib>Casagrande, Viviana</creatorcontrib><creatorcontrib>Mavilio, Maria</creatorcontrib><creatorcontrib>Sacchetta, Paolo</creatorcontrib><creatorcontrib>Federici, Massimo</creatorcontrib><creatorcontrib>Menghini, Rossella</creatorcontrib><creatorcontrib>Urbani, Andrea</creatorcontrib><creatorcontrib>Ciavardelli, Domenico</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</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 Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</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>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Acta diabetologica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Rossi, Claudia</au><au>Marzano, Valeria</au><au>Consalvo, Ada</au><au>Zucchelli, Mirco</au><au>Levi Mortera, Stefano</au><au>Casagrande, Viviana</au><au>Mavilio, Maria</au><au>Sacchetta, Paolo</au><au>Federici, Massimo</au><au>Menghini, Rossella</au><au>Urbani, Andrea</au><au>Ciavardelli, Domenico</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Proteomic and metabolomic characterization of streptozotocin-induced diabetic nephropathy in TIMP3-deficient mice</atitle><jtitle>Acta diabetologica</jtitle><stitle>Acta Diabetol</stitle><addtitle>Acta Diabetol</addtitle><date>2018-02-01</date><risdate>2018</risdate><volume>55</volume><issue>2</issue><spage>121</spage><epage>129</epage><pages>121-129</pages><issn>0940-5429</issn><eissn>1432-5233</eissn><abstract>Aims
The tissue inhibitor of metalloproteinase TIMP3 is a stromal protein that restrains the activity of both protease and receptor in the extracellular matrix and has been found to be down-regulated in diabetic nephropathy (DN), the leading cause of end-stage renal disease in developed countries.
Methods
In order to gain deeper insights on the association of loss of TIMP3 and DN, we performed differential proteomic analysis of kidney and blood metabolic profiling of wild-type and Timp3-knockout mice before and after streptozotocin (STZ) treatment, widely used to induce insulin deficiency and hyperglycemia.
Results
Kidney proteomic data and blood metabolic profiles suggest significant alterations of peroxisomal and mitochondrial fatty acids β-oxidation in Timp3-knockout mice compared to wild-type mice under basal condition. These alterations were exacerbated in response to STZ treatment.
Conclusions
Proteomic and metabolomic approaches showed that loss of TIMP3 alone or in combination with STZ treatment results in significant alterations of kidney lipid metabolism and peripheral acylcarnitine levels, supporting the idea that loss of TIMP3 may generate a phenotype more prone to DN.</abstract><cop>Milan</cop><pub>Springer Milan</pub><pmid>29134286</pmid><doi>10.1007/s00592-017-1074-y</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0003-0949-0280</orcidid><orcidid>https://orcid.org/0000-0002-1410-3946</orcidid><orcidid>https://orcid.org/0000-0003-4989-5194</orcidid><orcidid>https://orcid.org/0000-0002-1087-847X</orcidid><orcidid>https://orcid.org/0000-0001-6184-0933</orcidid><orcidid>https://orcid.org/0000-0001-8397-2355</orcidid><orcidid>https://orcid.org/0000-0001-9168-3174</orcidid><orcidid>https://orcid.org/0000-0003-3860-9404</orcidid><orcidid>https://orcid.org/0000-0001-6364-2121</orcidid></addata></record> |
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| ispartof | Acta diabetologica, 2018-02, Vol.55 (2), p.121-129 |
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| subjects | Animals Diabetes Diabetes mellitus Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - complications Diabetes Mellitus, Experimental - metabolism Diabetic Nephropathies - chemically induced Diabetic Nephropathies - genetics Diabetic Nephropathies - metabolism Diabetic Nephropathies - pathology Diabetic nephropathy End-stage renal disease Extracellular matrix Fatty acids Hyperglycemia Insulin Internal Medicine Kidney - metabolism Kidney diseases Kidney Failure, Chronic - chemically induced Kidney Failure, Chronic - genetics Kidney Failure, Chronic - metabolism Kidney Failure, Chronic - pathology Lipid Metabolism Medicine Medicine & Public Health Metabolic Diseases Metabolism Metabolome Metabolomics Metalloproteinase Mice Mice, Inbred C57BL Mice, Knockout Mitochondria Nephropathy Original Article Oxidation Proteome - analysis Proteome - metabolism Proteomics Rodents Streptozocin Tissue inhibitor of metalloproteinase 3 Tissue Inhibitor of Metalloproteinase-3 - genetics |
| title | Proteomic and metabolomic characterization of streptozotocin-induced diabetic nephropathy in TIMP3-deficient mice |
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