MicroRNA‐7a‐5p ameliorates diabetic peripheral neuropathy by regulating VDAC1/JNK/c‐JUN pathway
Aims The pathogenesis of diabetic peripheral neuropathy (DPN) is complex, and its treatment is extremely challenging. MicroRNA‐7a‐5p (miR‐7a‐5p) has been widely reported to alleviate apoptosis and oxidative stress in various diseases. This study aimed to investigate the mechanism of miR‐7a‐5p in DPN...
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| Veröffentlicht in: | Diabetic medicine 2023-01, Vol.40 (1), p.e14890-n/a |
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| creator | Jiao, Yang Zhang, Yue‐Hua Wang, Chun‐Yan Yu, Yang Li, Yi‐Ze Cui, Wei Li, Qing Yu, Yong‐Hao |
| description | Aims
The pathogenesis of diabetic peripheral neuropathy (DPN) is complex, and its treatment is extremely challenging. MicroRNA‐7a‐5p (miR‐7a‐5p) has been widely reported to alleviate apoptosis and oxidative stress in various diseases. This study aimed to investigate the mechanism of miR‐7a‐5p in DPN.
Methods
DPN cell model was constructed with high‐glucose–induced RSC96 cells. Cell apoptosis and viability were detected by flow cytometry analysis and cell counting kit‐8 (CCK‐8) assay respectively. The apoptosis and Jun N‐terminal kinase (JNK)/c‐JUN signalling pathway‐related proteins expression were detected by Western blotting. The intracellular calcium content and oxidative stress levels were detected by flow cytometry and reagent kits. Mitochondrial membrane potential was evaluated by tetrechloro‐tetraethylbenzimidazol carbocyanine iodide (JC‐1) staining. The targeting relationship between miR‐7a‐5p and voltage‐dependent anion‐selective channel protein 1 (VDAC1) was determined by RNA pull‐down assay and dual‐luciferase reporter gene assay. The streptozotocin (STZ) rat model was constructed to simulate DPN in vivo. The paw withdrawal mechanical threshold (PTW) was measured by Frey capillary line, and the motor nerve conduction velocity (MNCV) was measured by electromyography.
Results
MiR‐7a‐5p expression was decreased, while VDAC1 expression was increased in HG‐induced RSC96 cells and STZ rats. In HG‐induced RSC96 cells, miR‐7a‐5p overexpression promoted cell proliferation, inhibited apoptosis, down‐regulated calcium release, improved mitochondrial membrane potential and repressed oxidative stress response. MiR‐7a‐5p negatively regulated VDAC1 expression. VDAC1 knockdown improved cell proliferation activity, suppressed cell apoptosis and mitochondrial dysfunction by inhibiting JNK/c‐JUN pathway activation. MiR‐7a‐5p overexpression raised PTW, restored MNCV and reduced oxidative stress levels and nerve cell apoptosis in STZ rats.
Conclusion
MiR‐7a‐5p overexpression ameliorated mitochondrial dysfunction and inhibited apoptosis in DPN by regulating VDAC1/JNK/c‐JUN pathway. |
| doi_str_mv | 10.1111/dme.14890 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2670063950</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2755145797</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3530-90f051727ef22b3e07aae2fa7b11614876d05763743433b9c52d3560f8066e133</originalsourceid><addsrcrecordid>eNp1kMtO3DAUQC1UBFPaRX-gitRNuwhz_cbL0UB5T6WqsLWc5AaMkkmwE6Hs-gn9Rr4Ew0AXlXoXvpujI99DyCcK-zTNvGpxn4oDA1tkRoUSuRSGviMz0ILlHDTdJe9jvAOgzHCzQ3a5VFQZYWYEL30Zup-rxePvP9qlR_aZa7HxXXADxqzyrsDBl1mPwfe3GFyTrXEMXe-G2ykrpizgzdi4wa9vsuvDxZLOz1bn8zKZzq5W2TP14KYPZLt2TcSPr3uPXH0_-rU8yS9-HJ8uFxd5ySWH3EANkmqmsWas4AjaOWS10wWlKh2oVQVSK64FF5wXppSsSqdAfQBKIeV8j3zdePvQ3Y8YB9v6WGLTuDV2Y7RMaQDFjYSEfvkHvevGsE6_s0xLSYXURifq24ZKkWIMWNs--NaFyVKwz-1tam9f2if286txLFqs_pJvsRMw3wAPvsHp_yZ7eHm0UT4B1WONag</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2755145797</pqid></control><display><type>article</type><title>MicroRNA‐7a‐5p ameliorates diabetic peripheral neuropathy by regulating VDAC1/JNK/c‐JUN pathway</title><source>MEDLINE</source><source>Wiley Online Library All Journals</source><creator>Jiao, Yang ; Zhang, Yue‐Hua ; Wang, Chun‐Yan ; Yu, Yang ; Li, Yi‐Ze ; Cui, Wei ; Li, Qing ; Yu, Yong‐Hao</creator><creatorcontrib>Jiao, Yang ; Zhang, Yue‐Hua ; Wang, Chun‐Yan ; Yu, Yang ; Li, Yi‐Ze ; Cui, Wei ; Li, Qing ; Yu, Yong‐Hao</creatorcontrib><description>Aims
The pathogenesis of diabetic peripheral neuropathy (DPN) is complex, and its treatment is extremely challenging. MicroRNA‐7a‐5p (miR‐7a‐5p) has been widely reported to alleviate apoptosis and oxidative stress in various diseases. This study aimed to investigate the mechanism of miR‐7a‐5p in DPN.
Methods
DPN cell model was constructed with high‐glucose–induced RSC96 cells. Cell apoptosis and viability were detected by flow cytometry analysis and cell counting kit‐8 (CCK‐8) assay respectively. The apoptosis and Jun N‐terminal kinase (JNK)/c‐JUN signalling pathway‐related proteins expression were detected by Western blotting. The intracellular calcium content and oxidative stress levels were detected by flow cytometry and reagent kits. Mitochondrial membrane potential was evaluated by tetrechloro‐tetraethylbenzimidazol carbocyanine iodide (JC‐1) staining. The targeting relationship between miR‐7a‐5p and voltage‐dependent anion‐selective channel protein 1 (VDAC1) was determined by RNA pull‐down assay and dual‐luciferase reporter gene assay. The streptozotocin (STZ) rat model was constructed to simulate DPN in vivo. The paw withdrawal mechanical threshold (PTW) was measured by Frey capillary line, and the motor nerve conduction velocity (MNCV) was measured by electromyography.
Results
MiR‐7a‐5p expression was decreased, while VDAC1 expression was increased in HG‐induced RSC96 cells and STZ rats. In HG‐induced RSC96 cells, miR‐7a‐5p overexpression promoted cell proliferation, inhibited apoptosis, down‐regulated calcium release, improved mitochondrial membrane potential and repressed oxidative stress response. MiR‐7a‐5p negatively regulated VDAC1 expression. VDAC1 knockdown improved cell proliferation activity, suppressed cell apoptosis and mitochondrial dysfunction by inhibiting JNK/c‐JUN pathway activation. MiR‐7a‐5p overexpression raised PTW, restored MNCV and reduced oxidative stress levels and nerve cell apoptosis in STZ rats.
Conclusion
MiR‐7a‐5p overexpression ameliorated mitochondrial dysfunction and inhibited apoptosis in DPN by regulating VDAC1/JNK/c‐JUN pathway.</description><identifier>ISSN: 0742-3071</identifier><identifier>EISSN: 1464-5491</identifier><identifier>DOI: 10.1111/dme.14890</identifier><identifier>PMID: 35616949</identifier><language>eng</language><publisher>England: Wiley Subscription Services, Inc</publisher><subject>Animals ; Apoptosis ; Calcium (intracellular) ; Calcium (mitochondrial) ; Calcium - adverse effects ; Calcium - metabolism ; Cell growth ; Cell proliferation ; Cellular stress response ; Cholecystokinin ; Diabetes ; Diabetes mellitus ; Diabetes Mellitus, Experimental ; Diabetic Neuropathies - genetics ; Diabetic Neuropathies - pathology ; diabetic peripheral neuropathy ; Electromyography ; Flow cytometry ; Intracellular signalling ; JNK/c‐JUN pathway ; Kinases ; Membrane potential ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; MiR‐7a‐5p ; Mitochondria ; mitochondrial dysfunction ; Nerve conduction ; Oxidative stress ; Peripheral neuropathy ; Rats ; Reporter gene ; RSC96 cells ; Signal transduction ; Streptozocin ; VDAC1 ; Voltage-Dependent Anion Channel 1 ; Western blotting</subject><ispartof>Diabetic medicine, 2023-01, Vol.40 (1), p.e14890-n/a</ispartof><rights>2022 Diabetes UK.</rights><rights>Diabetic Medicine © 2023 Diabetes UK</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3530-90f051727ef22b3e07aae2fa7b11614876d05763743433b9c52d3560f8066e133</citedby><cites>FETCH-LOGICAL-c3530-90f051727ef22b3e07aae2fa7b11614876d05763743433b9c52d3560f8066e133</cites><orcidid>0000-0001-9111-6129</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fdme.14890$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fdme.14890$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27929,27930,45579,45580</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35616949$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiao, Yang</creatorcontrib><creatorcontrib>Zhang, Yue‐Hua</creatorcontrib><creatorcontrib>Wang, Chun‐Yan</creatorcontrib><creatorcontrib>Yu, Yang</creatorcontrib><creatorcontrib>Li, Yi‐Ze</creatorcontrib><creatorcontrib>Cui, Wei</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Yu, Yong‐Hao</creatorcontrib><title>MicroRNA‐7a‐5p ameliorates diabetic peripheral neuropathy by regulating VDAC1/JNK/c‐JUN pathway</title><title>Diabetic medicine</title><addtitle>Diabet Med</addtitle><description>Aims
The pathogenesis of diabetic peripheral neuropathy (DPN) is complex, and its treatment is extremely challenging. MicroRNA‐7a‐5p (miR‐7a‐5p) has been widely reported to alleviate apoptosis and oxidative stress in various diseases. This study aimed to investigate the mechanism of miR‐7a‐5p in DPN.
Methods
DPN cell model was constructed with high‐glucose–induced RSC96 cells. Cell apoptosis and viability were detected by flow cytometry analysis and cell counting kit‐8 (CCK‐8) assay respectively. The apoptosis and Jun N‐terminal kinase (JNK)/c‐JUN signalling pathway‐related proteins expression were detected by Western blotting. The intracellular calcium content and oxidative stress levels were detected by flow cytometry and reagent kits. Mitochondrial membrane potential was evaluated by tetrechloro‐tetraethylbenzimidazol carbocyanine iodide (JC‐1) staining. The targeting relationship between miR‐7a‐5p and voltage‐dependent anion‐selective channel protein 1 (VDAC1) was determined by RNA pull‐down assay and dual‐luciferase reporter gene assay. The streptozotocin (STZ) rat model was constructed to simulate DPN in vivo. The paw withdrawal mechanical threshold (PTW) was measured by Frey capillary line, and the motor nerve conduction velocity (MNCV) was measured by electromyography.
Results
MiR‐7a‐5p expression was decreased, while VDAC1 expression was increased in HG‐induced RSC96 cells and STZ rats. In HG‐induced RSC96 cells, miR‐7a‐5p overexpression promoted cell proliferation, inhibited apoptosis, down‐regulated calcium release, improved mitochondrial membrane potential and repressed oxidative stress response. MiR‐7a‐5p negatively regulated VDAC1 expression. VDAC1 knockdown improved cell proliferation activity, suppressed cell apoptosis and mitochondrial dysfunction by inhibiting JNK/c‐JUN pathway activation. MiR‐7a‐5p overexpression raised PTW, restored MNCV and reduced oxidative stress levels and nerve cell apoptosis in STZ rats.
Conclusion
MiR‐7a‐5p overexpression ameliorated mitochondrial dysfunction and inhibited apoptosis in DPN by regulating VDAC1/JNK/c‐JUN pathway.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Calcium (intracellular)</subject><subject>Calcium (mitochondrial)</subject><subject>Calcium - adverse effects</subject><subject>Calcium - metabolism</subject><subject>Cell growth</subject><subject>Cell proliferation</subject><subject>Cellular stress response</subject><subject>Cholecystokinin</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetes Mellitus, Experimental</subject><subject>Diabetic Neuropathies - genetics</subject><subject>Diabetic Neuropathies - pathology</subject><subject>diabetic peripheral neuropathy</subject><subject>Electromyography</subject><subject>Flow cytometry</subject><subject>Intracellular signalling</subject><subject>JNK/c‐JUN pathway</subject><subject>Kinases</subject><subject>Membrane potential</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>MiR‐7a‐5p</subject><subject>Mitochondria</subject><subject>mitochondrial dysfunction</subject><subject>Nerve conduction</subject><subject>Oxidative stress</subject><subject>Peripheral neuropathy</subject><subject>Rats</subject><subject>Reporter gene</subject><subject>RSC96 cells</subject><subject>Signal transduction</subject><subject>Streptozocin</subject><subject>VDAC1</subject><subject>Voltage-Dependent Anion Channel 1</subject><subject>Western blotting</subject><issn>0742-3071</issn><issn>1464-5491</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtO3DAUQC1UBFPaRX-gitRNuwhz_cbL0UB5T6WqsLWc5AaMkkmwE6Hs-gn9Rr4Ew0AXlXoXvpujI99DyCcK-zTNvGpxn4oDA1tkRoUSuRSGviMz0ILlHDTdJe9jvAOgzHCzQ3a5VFQZYWYEL30Zup-rxePvP9qlR_aZa7HxXXADxqzyrsDBl1mPwfe3GFyTrXEMXe-G2ykrpizgzdi4wa9vsuvDxZLOz1bn8zKZzq5W2TP14KYPZLt2TcSPr3uPXH0_-rU8yS9-HJ8uFxd5ySWH3EANkmqmsWas4AjaOWS10wWlKh2oVQVSK64FF5wXppSsSqdAfQBKIeV8j3zdePvQ3Y8YB9v6WGLTuDV2Y7RMaQDFjYSEfvkHvevGsE6_s0xLSYXURifq24ZKkWIMWNs--NaFyVKwz-1tam9f2if286txLFqs_pJvsRMw3wAPvsHp_yZ7eHm0UT4B1WONag</recordid><startdate>202301</startdate><enddate>202301</enddate><creator>Jiao, Yang</creator><creator>Zhang, Yue‐Hua</creator><creator>Wang, Chun‐Yan</creator><creator>Yu, Yang</creator><creator>Li, Yi‐Ze</creator><creator>Cui, Wei</creator><creator>Li, Qing</creator><creator>Yu, Yong‐Hao</creator><general>Wiley Subscription Services, 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>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-9111-6129</orcidid></search><sort><creationdate>202301</creationdate><title>MicroRNA‐7a‐5p ameliorates diabetic peripheral neuropathy by regulating VDAC1/JNK/c‐JUN pathway</title><author>Jiao, Yang ; Zhang, Yue‐Hua ; Wang, Chun‐Yan ; Yu, Yang ; Li, Yi‐Ze ; Cui, Wei ; Li, Qing ; Yu, Yong‐Hao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3530-90f051727ef22b3e07aae2fa7b11614876d05763743433b9c52d3560f8066e133</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Calcium (intracellular)</topic><topic>Calcium (mitochondrial)</topic><topic>Calcium - adverse effects</topic><topic>Calcium - metabolism</topic><topic>Cell growth</topic><topic>Cell proliferation</topic><topic>Cellular stress response</topic><topic>Cholecystokinin</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetes Mellitus, Experimental</topic><topic>Diabetic Neuropathies - genetics</topic><topic>Diabetic Neuropathies - pathology</topic><topic>diabetic peripheral neuropathy</topic><topic>Electromyography</topic><topic>Flow cytometry</topic><topic>Intracellular signalling</topic><topic>JNK/c‐JUN pathway</topic><topic>Kinases</topic><topic>Membrane potential</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>MiR‐7a‐5p</topic><topic>Mitochondria</topic><topic>mitochondrial dysfunction</topic><topic>Nerve conduction</topic><topic>Oxidative stress</topic><topic>Peripheral neuropathy</topic><topic>Rats</topic><topic>Reporter gene</topic><topic>RSC96 cells</topic><topic>Signal transduction</topic><topic>Streptozocin</topic><topic>VDAC1</topic><topic>Voltage-Dependent Anion Channel 1</topic><topic>Western blotting</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiao, Yang</creatorcontrib><creatorcontrib>Zhang, Yue‐Hua</creatorcontrib><creatorcontrib>Wang, Chun‐Yan</creatorcontrib><creatorcontrib>Yu, Yang</creatorcontrib><creatorcontrib>Li, Yi‐Ze</creatorcontrib><creatorcontrib>Cui, Wei</creatorcontrib><creatorcontrib>Li, Qing</creatorcontrib><creatorcontrib>Yu, Yong‐Hao</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Diabetic medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiao, Yang</au><au>Zhang, Yue‐Hua</au><au>Wang, Chun‐Yan</au><au>Yu, Yang</au><au>Li, Yi‐Ze</au><au>Cui, Wei</au><au>Li, Qing</au><au>Yu, Yong‐Hao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA‐7a‐5p ameliorates diabetic peripheral neuropathy by regulating VDAC1/JNK/c‐JUN pathway</atitle><jtitle>Diabetic medicine</jtitle><addtitle>Diabet Med</addtitle><date>2023-01</date><risdate>2023</risdate><volume>40</volume><issue>1</issue><spage>e14890</spage><epage>n/a</epage><pages>e14890-n/a</pages><issn>0742-3071</issn><eissn>1464-5491</eissn><abstract>Aims
The pathogenesis of diabetic peripheral neuropathy (DPN) is complex, and its treatment is extremely challenging. MicroRNA‐7a‐5p (miR‐7a‐5p) has been widely reported to alleviate apoptosis and oxidative stress in various diseases. This study aimed to investigate the mechanism of miR‐7a‐5p in DPN.
Methods
DPN cell model was constructed with high‐glucose–induced RSC96 cells. Cell apoptosis and viability were detected by flow cytometry analysis and cell counting kit‐8 (CCK‐8) assay respectively. The apoptosis and Jun N‐terminal kinase (JNK)/c‐JUN signalling pathway‐related proteins expression were detected by Western blotting. The intracellular calcium content and oxidative stress levels were detected by flow cytometry and reagent kits. Mitochondrial membrane potential was evaluated by tetrechloro‐tetraethylbenzimidazol carbocyanine iodide (JC‐1) staining. The targeting relationship between miR‐7a‐5p and voltage‐dependent anion‐selective channel protein 1 (VDAC1) was determined by RNA pull‐down assay and dual‐luciferase reporter gene assay. The streptozotocin (STZ) rat model was constructed to simulate DPN in vivo. The paw withdrawal mechanical threshold (PTW) was measured by Frey capillary line, and the motor nerve conduction velocity (MNCV) was measured by electromyography.
Results
MiR‐7a‐5p expression was decreased, while VDAC1 expression was increased in HG‐induced RSC96 cells and STZ rats. In HG‐induced RSC96 cells, miR‐7a‐5p overexpression promoted cell proliferation, inhibited apoptosis, down‐regulated calcium release, improved mitochondrial membrane potential and repressed oxidative stress response. MiR‐7a‐5p negatively regulated VDAC1 expression. VDAC1 knockdown improved cell proliferation activity, suppressed cell apoptosis and mitochondrial dysfunction by inhibiting JNK/c‐JUN pathway activation. MiR‐7a‐5p overexpression raised PTW, restored MNCV and reduced oxidative stress levels and nerve cell apoptosis in STZ rats.
Conclusion
MiR‐7a‐5p overexpression ameliorated mitochondrial dysfunction and inhibited apoptosis in DPN by regulating VDAC1/JNK/c‐JUN pathway.</abstract><cop>England</cop><pub>Wiley Subscription Services, Inc</pub><pmid>35616949</pmid><doi>10.1111/dme.14890</doi><tpages>17</tpages><orcidid>https://orcid.org/0000-0001-9111-6129</orcidid></addata></record> |
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| subjects | Animals Apoptosis Calcium (intracellular) Calcium (mitochondrial) Calcium - adverse effects Calcium - metabolism Cell growth Cell proliferation Cellular stress response Cholecystokinin Diabetes Diabetes mellitus Diabetes Mellitus, Experimental Diabetic Neuropathies - genetics Diabetic Neuropathies - pathology diabetic peripheral neuropathy Electromyography Flow cytometry Intracellular signalling JNK/c‐JUN pathway Kinases Membrane potential MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA MiR‐7a‐5p Mitochondria mitochondrial dysfunction Nerve conduction Oxidative stress Peripheral neuropathy Rats Reporter gene RSC96 cells Signal transduction Streptozocin VDAC1 Voltage-Dependent Anion Channel 1 Western blotting |
| title | MicroRNA‐7a‐5p ameliorates diabetic peripheral neuropathy by regulating VDAC1/JNK/c‐JUN pathway |
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