A sodium-glucose cotransporter 2 inhibitor attenuates renal capillary injury and fibrosis by a vascular endothelial growth factor–dependent pathway after renal injury in mice
Multiple large clinical trials have shown that sodium-glucose cotransporter (SGLT) 2 inhibitors reduce the risk of renal events. However, the mechanism responsible for this outcome remains unknown. Here we investigated the effects of the SGLT2 inhibitor luseogliflozin on the development of renal fib...
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| Veröffentlicht in: | Kidney international 2018-09, Vol.94 (3), p.524-535 |
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| creator | Zhang, Yifan Nakano, Daisuke Guan, Yu Hitomi, Hirofumi Uemura, Akiyoshi Masaki, Tsutomu Kobara, Hideki Sugaya, Takeshi Nishiyama, Akira |
| description | Multiple large clinical trials have shown that sodium-glucose cotransporter (SGLT) 2 inhibitors reduce the risk of renal events. However, the mechanism responsible for this outcome remains unknown. Here we investigated the effects of the SGLT2 inhibitor luseogliflozin on the development of renal fibrosis after renal ischemia/reperfusion injury in non-diabetic mice. Luseogliflozin significantly suppressed development of renal fibrosis, prevented peritubular capillary congestion/hemorrhage, attenuated CD31-positive cell loss, suppressed hypoxia, and increased vascular endothelial growth factor (VEGF)-A expression in the kidney after ischemia/reperfusion injury. Luseogliflozin failed to induce the above-mentioned protection in animals co-treated with sunitinib, a VEGF receptor inhibitor. Additionally, luseogliflozin reduced glucose uptake and increased VEGF-A expression in the kidneys of glucose transporter 2 (GLUT2)-downregulated mice following ischemia/reperfusion and in GLUT2-knock-down cells compared with those in normal controls. Withdrawal of glucose from cultured medium, to halt glucose uptake, remarkably increased VEGF-A expression and reversed the luseogliflozin-induced increase in VEGF-A expression in the proximal tubular cells. Thus, luseogliflozin prevented endothelial rarefaction and subsequent renal fibrosis after renal ischemia/reperfusion injury through a VEGF-dependent pathway induced by the dysfunction of proximal tubular glucose uptake in tubules with injury-induced GLUT2 downregulation.
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| doi_str_mv | 10.1016/j.kint.2018.05.002 |
| format | Article |
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[Display omitted]</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1016/j.kint.2018.05.002</identifier><identifier>PMID: 30045814</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acute Kidney Injury - drug therapy ; Acute Kidney Injury - etiology ; Acute Kidney Injury - pathology ; Angiogenesis Inhibitors - pharmacology ; Animals ; Blood Glucose - metabolism ; Capillaries - drug effects ; Capillaries - metabolism ; Capillaries - pathology ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Fibrosis ; Gene Knockdown Techniques ; Glucose Transporter Type 2 - genetics ; Glucose Transporter Type 2 - metabolism ; glucose uptake ; Humans ; Kidney Tubules, Proximal - blood supply ; Kidney Tubules, Proximal - drug effects ; Kidney Tubules, Proximal - metabolism ; Kidney Tubules, Proximal - pathology ; Male ; Mice ; Mice, Inbred C57BL ; Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors ; renal fibrosis ; Reperfusion Injury - complications ; Reperfusion Injury - pathology ; sodium glucose co-transporter 2 ; Sodium-Glucose Transporter 2 - metabolism ; Sodium-Glucose Transporter 2 Inhibitors - pharmacology ; Sodium-Glucose Transporter 2 Inhibitors - therapeutic use ; Sorbitol - analogs & derivatives ; Sorbitol - pharmacology ; Sorbitol - therapeutic use ; Sunitinib - pharmacology ; Treatment Outcome ; vascular endothelial growth factor ; Vascular Endothelial Growth Factor A - metabolism</subject><ispartof>Kidney international, 2018-09, Vol.94 (3), p.524-535</ispartof><rights>2018 International Society of Nephrology</rights><rights>Copyright © 2018 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c466t-4aae085d36994e9251f89eac049d382e5a53ce568260ed796c5f947eeb74e6bc3</citedby><cites>FETCH-LOGICAL-c466t-4aae085d36994e9251f89eac049d382e5a53ce568260ed796c5f947eeb74e6bc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30045814$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Yifan</creatorcontrib><creatorcontrib>Nakano, Daisuke</creatorcontrib><creatorcontrib>Guan, Yu</creatorcontrib><creatorcontrib>Hitomi, Hirofumi</creatorcontrib><creatorcontrib>Uemura, Akiyoshi</creatorcontrib><creatorcontrib>Masaki, Tsutomu</creatorcontrib><creatorcontrib>Kobara, Hideki</creatorcontrib><creatorcontrib>Sugaya, Takeshi</creatorcontrib><creatorcontrib>Nishiyama, Akira</creatorcontrib><title>A sodium-glucose cotransporter 2 inhibitor attenuates renal capillary injury and fibrosis by a vascular endothelial growth factor–dependent pathway after renal injury in mice</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Multiple large clinical trials have shown that sodium-glucose cotransporter (SGLT) 2 inhibitors reduce the risk of renal events. However, the mechanism responsible for this outcome remains unknown. Here we investigated the effects of the SGLT2 inhibitor luseogliflozin on the development of renal fibrosis after renal ischemia/reperfusion injury in non-diabetic mice. Luseogliflozin significantly suppressed development of renal fibrosis, prevented peritubular capillary congestion/hemorrhage, attenuated CD31-positive cell loss, suppressed hypoxia, and increased vascular endothelial growth factor (VEGF)-A expression in the kidney after ischemia/reperfusion injury. Luseogliflozin failed to induce the above-mentioned protection in animals co-treated with sunitinib, a VEGF receptor inhibitor. Additionally, luseogliflozin reduced glucose uptake and increased VEGF-A expression in the kidneys of glucose transporter 2 (GLUT2)-downregulated mice following ischemia/reperfusion and in GLUT2-knock-down cells compared with those in normal controls. Withdrawal of glucose from cultured medium, to halt glucose uptake, remarkably increased VEGF-A expression and reversed the luseogliflozin-induced increase in VEGF-A expression in the proximal tubular cells. Thus, luseogliflozin prevented endothelial rarefaction and subsequent renal fibrosis after renal ischemia/reperfusion injury through a VEGF-dependent pathway induced by the dysfunction of proximal tubular glucose uptake in tubules with injury-induced GLUT2 downregulation.
[Display omitted]</description><subject>Acute Kidney Injury - drug therapy</subject><subject>Acute Kidney Injury - etiology</subject><subject>Acute Kidney Injury - pathology</subject><subject>Angiogenesis Inhibitors - pharmacology</subject><subject>Animals</subject><subject>Blood Glucose - metabolism</subject><subject>Capillaries - drug effects</subject><subject>Capillaries - metabolism</subject><subject>Capillaries - pathology</subject><subject>Disease Models, Animal</subject><subject>Drug Evaluation, Preclinical</subject><subject>Fibrosis</subject><subject>Gene Knockdown Techniques</subject><subject>Glucose Transporter Type 2 - genetics</subject><subject>Glucose Transporter Type 2 - metabolism</subject><subject>glucose uptake</subject><subject>Humans</subject><subject>Kidney Tubules, Proximal - blood supply</subject><subject>Kidney Tubules, Proximal - drug effects</subject><subject>Kidney Tubules, Proximal - metabolism</subject><subject>Kidney Tubules, Proximal - pathology</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors</subject><subject>renal fibrosis</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - pathology</subject><subject>sodium glucose co-transporter 2</subject><subject>Sodium-Glucose Transporter 2 - metabolism</subject><subject>Sodium-Glucose Transporter 2 Inhibitors - pharmacology</subject><subject>Sodium-Glucose Transporter 2 Inhibitors - therapeutic use</subject><subject>Sorbitol - analogs & derivatives</subject><subject>Sorbitol - pharmacology</subject><subject>Sorbitol - therapeutic use</subject><subject>Sunitinib - pharmacology</subject><subject>Treatment Outcome</subject><subject>vascular endothelial growth factor</subject><subject>Vascular Endothelial Growth Factor A - metabolism</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc2OFCEUhYnROO3oC7gwLN1UCRRQVOJmMhl_kknc6JpQcGuatgpKoGbiznfwRXwmn0Q63bp0dXPDd87N4SD0kpKWEirfHNqvPpSWEapaIlpC2CO0o4J1De2FeIx2hCjRMNGpC_Qs5wOp-9CRp-iiI4QLRfkO_brCOTq_Lc3dvNmYAdtYkgl5jalAwgz7sPejLzFhUwqEzRTIOEEwM7Zm9fNs0vcKHbY6THB48mOK2Wc81h3fm2y3imAILpY9zL7q7lJ8KHs8GVttf__46WCtzxAKXk3ZP5gqnI7HT1fO3j7gxVt4jp5MZs7w4jwv0Zd3N5-vPzS3n95_vL66bSyXsjTcGKjpXSeHgcPABJ3UAMYSPrhOMRBGdBaEVEwScP0grZgG3gOMPQc52u4SvT75ril-2yAXvfhsocYNELesGemlUmroeUXZCbU1eE4w6TX5pX6LpkQfm9IHfWxKH5vSROjaVBW9Ovtv4wLun-RvNRV4ewKgprz3kHS2HoIF5xPYol30__P_AwDBqwc</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Zhang, Yifan</creator><creator>Nakano, Daisuke</creator><creator>Guan, Yu</creator><creator>Hitomi, Hirofumi</creator><creator>Uemura, Akiyoshi</creator><creator>Masaki, Tsutomu</creator><creator>Kobara, Hideki</creator><creator>Sugaya, Takeshi</creator><creator>Nishiyama, Akira</creator><general>Elsevier Inc</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>7X8</scope></search><sort><creationdate>201809</creationdate><title>A sodium-glucose cotransporter 2 inhibitor attenuates renal capillary injury and fibrosis by a vascular endothelial growth factor–dependent pathway after renal injury in mice</title><author>Zhang, Yifan ; Nakano, Daisuke ; Guan, Yu ; Hitomi, Hirofumi ; Uemura, Akiyoshi ; Masaki, Tsutomu ; Kobara, Hideki ; Sugaya, Takeshi ; Nishiyama, Akira</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c466t-4aae085d36994e9251f89eac049d382e5a53ce568260ed796c5f947eeb74e6bc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Acute Kidney Injury - drug therapy</topic><topic>Acute Kidney Injury - etiology</topic><topic>Acute Kidney Injury - pathology</topic><topic>Angiogenesis Inhibitors - pharmacology</topic><topic>Animals</topic><topic>Blood Glucose - metabolism</topic><topic>Capillaries - drug effects</topic><topic>Capillaries - metabolism</topic><topic>Capillaries - pathology</topic><topic>Disease Models, Animal</topic><topic>Drug Evaluation, Preclinical</topic><topic>Fibrosis</topic><topic>Gene Knockdown Techniques</topic><topic>Glucose Transporter Type 2 - genetics</topic><topic>Glucose Transporter Type 2 - metabolism</topic><topic>glucose uptake</topic><topic>Humans</topic><topic>Kidney Tubules, Proximal - blood supply</topic><topic>Kidney Tubules, Proximal - drug effects</topic><topic>Kidney Tubules, Proximal - metabolism</topic><topic>Kidney Tubules, Proximal - pathology</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors</topic><topic>renal fibrosis</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - pathology</topic><topic>sodium glucose co-transporter 2</topic><topic>Sodium-Glucose Transporter 2 - metabolism</topic><topic>Sodium-Glucose Transporter 2 Inhibitors - pharmacology</topic><topic>Sodium-Glucose Transporter 2 Inhibitors - therapeutic use</topic><topic>Sorbitol - analogs & derivatives</topic><topic>Sorbitol - pharmacology</topic><topic>Sorbitol - therapeutic use</topic><topic>Sunitinib - pharmacology</topic><topic>Treatment Outcome</topic><topic>vascular endothelial growth factor</topic><topic>Vascular Endothelial Growth Factor A - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Yifan</creatorcontrib><creatorcontrib>Nakano, Daisuke</creatorcontrib><creatorcontrib>Guan, Yu</creatorcontrib><creatorcontrib>Hitomi, Hirofumi</creatorcontrib><creatorcontrib>Uemura, Akiyoshi</creatorcontrib><creatorcontrib>Masaki, Tsutomu</creatorcontrib><creatorcontrib>Kobara, Hideki</creatorcontrib><creatorcontrib>Sugaya, Takeshi</creatorcontrib><creatorcontrib>Nishiyama, Akira</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Yifan</au><au>Nakano, Daisuke</au><au>Guan, Yu</au><au>Hitomi, Hirofumi</au><au>Uemura, Akiyoshi</au><au>Masaki, Tsutomu</au><au>Kobara, Hideki</au><au>Sugaya, Takeshi</au><au>Nishiyama, Akira</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A sodium-glucose cotransporter 2 inhibitor attenuates renal capillary injury and fibrosis by a vascular endothelial growth factor–dependent pathway after renal injury in mice</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2018-09</date><risdate>2018</risdate><volume>94</volume><issue>3</issue><spage>524</spage><epage>535</epage><pages>524-535</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><abstract>Multiple large clinical trials have shown that sodium-glucose cotransporter (SGLT) 2 inhibitors reduce the risk of renal events. However, the mechanism responsible for this outcome remains unknown. Here we investigated the effects of the SGLT2 inhibitor luseogliflozin on the development of renal fibrosis after renal ischemia/reperfusion injury in non-diabetic mice. Luseogliflozin significantly suppressed development of renal fibrosis, prevented peritubular capillary congestion/hemorrhage, attenuated CD31-positive cell loss, suppressed hypoxia, and increased vascular endothelial growth factor (VEGF)-A expression in the kidney after ischemia/reperfusion injury. Luseogliflozin failed to induce the above-mentioned protection in animals co-treated with sunitinib, a VEGF receptor inhibitor. Additionally, luseogliflozin reduced glucose uptake and increased VEGF-A expression in the kidneys of glucose transporter 2 (GLUT2)-downregulated mice following ischemia/reperfusion and in GLUT2-knock-down cells compared with those in normal controls. Withdrawal of glucose from cultured medium, to halt glucose uptake, remarkably increased VEGF-A expression and reversed the luseogliflozin-induced increase in VEGF-A expression in the proximal tubular cells. Thus, luseogliflozin prevented endothelial rarefaction and subsequent renal fibrosis after renal ischemia/reperfusion injury through a VEGF-dependent pathway induced by the dysfunction of proximal tubular glucose uptake in tubules with injury-induced GLUT2 downregulation.
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| subjects | Acute Kidney Injury - drug therapy Acute Kidney Injury - etiology Acute Kidney Injury - pathology Angiogenesis Inhibitors - pharmacology Animals Blood Glucose - metabolism Capillaries - drug effects Capillaries - metabolism Capillaries - pathology Disease Models, Animal Drug Evaluation, Preclinical Fibrosis Gene Knockdown Techniques Glucose Transporter Type 2 - genetics Glucose Transporter Type 2 - metabolism glucose uptake Humans Kidney Tubules, Proximal - blood supply Kidney Tubules, Proximal - drug effects Kidney Tubules, Proximal - metabolism Kidney Tubules, Proximal - pathology Male Mice Mice, Inbred C57BL Receptors, Vascular Endothelial Growth Factor - antagonists & inhibitors renal fibrosis Reperfusion Injury - complications Reperfusion Injury - pathology sodium glucose co-transporter 2 Sodium-Glucose Transporter 2 - metabolism Sodium-Glucose Transporter 2 Inhibitors - pharmacology Sodium-Glucose Transporter 2 Inhibitors - therapeutic use Sorbitol - analogs & derivatives Sorbitol - pharmacology Sorbitol - therapeutic use Sunitinib - pharmacology Treatment Outcome vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism |
| title | A sodium-glucose cotransporter 2 inhibitor attenuates renal capillary injury and fibrosis by a vascular endothelial growth factor–dependent pathway after renal injury in mice |
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