Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension
Significance: Hypertension has major health consequences, which is associated with endothelial dysfunction. Endothelial nitric oxide synthase (eNOS)-produced nitric oxide (NO) signaling in the vasculature plays an important role in maintaining vascular homeostasis. Considering the importance of NO s...
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| Veröffentlicht in: | Antioxidants & redox signaling 2021-03, Vol.34 (9), p.750-764 |
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| creator | Wu, Yin Ding, Ye Ramprasath, Tharmarajan Zou, Ming-Hui |
| description | Significance: Hypertension has major health consequences, which is associated with endothelial dysfunction. Endothelial nitric oxide synthase (eNOS)-produced nitric oxide (NO) signaling in the vasculature plays an important role in maintaining vascular homeostasis. Considering the importance of NO system, this review aims to provide a brief overview of the biochemistry of members of NO signaling, including GTPCH1 [guanosine 5 '-triphosphate (GTP) cyclohydrolase 1], tetrahydrobiopterin (BH4), and eNOS.
Recent Advances: Being NO signaling activators and regulators of eNOS signaling, BH4 treatment is getting widespread attention either as potential therapeutic agents or as preventive agents. Recent clinical trials also support that BH4 treatment could be considered a promising therapeutic in hypertension.
Critical Issues: Under conditions of BH4 depletion, eNOS-generated superoxides trigger pathological events. Abnormalities in NO availability and BH4 deficiency lead to disturbed redox regulation causing pathological events. This disturbed signaling influences the development of systemic hypertension as well as pulmonary hypertension.
Future Directions: Considering the importance of BH4 and NO to improve the translational significance, it is essential to continue research on this field to manipulate BH4 to increase the efficacy for treating hypertension. Thus, this review also examines the current state of knowledge on the effects of eNOS activators on preclinical models and humans to utilize this information for potential therapy. |
| doi_str_mv | 10.1089/ars.2020.8112 |
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Recent Advances: Being NO signaling activators and regulators of eNOS signaling, BH4 treatment is getting widespread attention either as potential therapeutic agents or as preventive agents. Recent clinical trials also support that BH4 treatment could be considered a promising therapeutic in hypertension.
Critical Issues: Under conditions of BH4 depletion, eNOS-generated superoxides trigger pathological events. Abnormalities in NO availability and BH4 deficiency lead to disturbed redox regulation causing pathological events. This disturbed signaling influences the development of systemic hypertension as well as pulmonary hypertension.
Future Directions: Considering the importance of BH4 and NO to improve the translational significance, it is essential to continue research on this field to manipulate BH4 to increase the efficacy for treating hypertension. Thus, this review also examines the current state of knowledge on the effects of eNOS activators on preclinical models and humans to utilize this information for potential therapy.</description><identifier>ISSN: 1523-0864</identifier><identifier>EISSN: 1557-7716</identifier><identifier>DOI: 10.1089/ars.2020.8112</identifier><identifier>PMID: 32363908</identifier><language>eng</language><publisher>NEW ROCHELLE: Mary Ann Liebert, Inc</publisher><subject>Abnormalities ; Biochemistry & Molecular Biology ; Biopterins - analogs & derivatives ; Biopterins - metabolism ; Chemical compounds ; Clinical trials ; Depletion ; Endocrinology & Metabolism ; Forum Review ; GTP Cyclohydrolase - genetics ; Homeostasis ; Humans ; Hypertension ; Hypertension (Ed. Bin Geng)—Part A ; Hypertension - genetics ; Hypertension - metabolism ; Hypertension - pathology ; Information processing ; Life Sciences & Biomedicine ; Nitric oxide ; Nitric Oxide - genetics ; Nitric Oxide - metabolism ; Nitric Oxide Synthase Type III - genetics ; Nitric Oxide Synthase Type III - metabolism ; Nitric-oxide synthase ; Oxidative stress ; Oxidative Stress - genetics ; Pharmacology ; Regulators ; Science & Technology ; Signal Transduction - genetics ; Signaling ; Tetrahydrobiopterin</subject><ispartof>Antioxidants & redox signaling, 2021-03, Vol.34 (9), p.750-764</ispartof><rights>Copyright Mary Ann Liebert, Inc. Mar 20, 2021</rights><rights>Copyright 2021, Mary Ann Liebert, Inc., publishers 2021 Mary Ann Liebert, Inc., publishers</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>56</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000538053000001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c415t-4d3f56b425fa027f52bbe8b529f58000d6266c8f9c51cb0afad1ca93f9a470c03</citedby><cites>FETCH-LOGICAL-c415t-4d3f56b425fa027f52bbe8b529f58000d6266c8f9c51cb0afad1ca93f9a470c03</cites><orcidid>0000-0002-2115-5875</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,781,785,886,27929,27930,39263</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32363908$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Yin</creatorcontrib><creatorcontrib>Ding, Ye</creatorcontrib><creatorcontrib>Ramprasath, Tharmarajan</creatorcontrib><creatorcontrib>Zou, Ming-Hui</creatorcontrib><title>Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension</title><title>Antioxidants & redox signaling</title><addtitle>ANTIOXID REDOX SIGN</addtitle><addtitle>Antioxid Redox Signal</addtitle><description>Significance: Hypertension has major health consequences, which is associated with endothelial dysfunction. Endothelial nitric oxide synthase (eNOS)-produced nitric oxide (NO) signaling in the vasculature plays an important role in maintaining vascular homeostasis. Considering the importance of NO system, this review aims to provide a brief overview of the biochemistry of members of NO signaling, including GTPCH1 [guanosine 5 '-triphosphate (GTP) cyclohydrolase 1], tetrahydrobiopterin (BH4), and eNOS.
Recent Advances: Being NO signaling activators and regulators of eNOS signaling, BH4 treatment is getting widespread attention either as potential therapeutic agents or as preventive agents. Recent clinical trials also support that BH4 treatment could be considered a promising therapeutic in hypertension.
Critical Issues: Under conditions of BH4 depletion, eNOS-generated superoxides trigger pathological events. Abnormalities in NO availability and BH4 deficiency lead to disturbed redox regulation causing pathological events. This disturbed signaling influences the development of systemic hypertension as well as pulmonary hypertension.
Future Directions: Considering the importance of BH4 and NO to improve the translational significance, it is essential to continue research on this field to manipulate BH4 to increase the efficacy for treating hypertension. Thus, this review also examines the current state of knowledge on the effects of eNOS activators on preclinical models and humans to utilize this information for potential therapy.</description><subject>Abnormalities</subject><subject>Biochemistry & Molecular Biology</subject><subject>Biopterins - analogs & derivatives</subject><subject>Biopterins - metabolism</subject><subject>Chemical compounds</subject><subject>Clinical trials</subject><subject>Depletion</subject><subject>Endocrinology & Metabolism</subject><subject>Forum Review</subject><subject>GTP Cyclohydrolase - genetics</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Hypertension</subject><subject>Hypertension (Ed. Bin Geng)—Part A</subject><subject>Hypertension - genetics</subject><subject>Hypertension - metabolism</subject><subject>Hypertension - pathology</subject><subject>Information processing</subject><subject>Life Sciences & Biomedicine</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - genetics</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase Type III - genetics</subject><subject>Nitric Oxide Synthase Type III - metabolism</subject><subject>Nitric-oxide synthase</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - genetics</subject><subject>Pharmacology</subject><subject>Regulators</subject><subject>Science & Technology</subject><subject>Signal Transduction - genetics</subject><subject>Signaling</subject><subject>Tetrahydrobiopterin</subject><issn>1523-0864</issn><issn>1557-7716</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><recordid>eNqNkc9rFDEUxwdR7A89epUBL4V21pdkMpNchDLUrlBawfbiJWQySTdlNlmTTHX_ezNsXdRTAyEP8smX9_IpincIFggY_yhDXGDAsGAI4RfFIaK0rdoWNS_nGpMKWFMfFEcxPgAARgheFwcEk4ZwYIfF95tfdpDJPuryWwo6xrPy8vZrt0RnpXRDeeEGn1Z6tHIsr20KVpXzgwxvXVrJqMs7p_y0Ga27L60rl9uNDkm7aL17U7wycoz67dN5XNx9vrjtltXVzeWX7vyqUjWiqaoHYmjT15gaCbg1FPe9Zj3F3FCWWx4a3DSKGa4oUj1IIwekJCeGy7oFBeS4-LTL3Uz9Wg9KuxTkKDbBrmXYCi-t-PfG2ZW494-i5Qhq1OaAk6eA4H9MOiaxtlHpcZRO-ykKTDhDDUBTZ_TDf-iDn4LL4wlccwJojsxUtaNU8DEGbfbNIBCzNZGtidmamK1l_v3fE-zpP5oycLoDfurem6isdkrvsfxJlLC8YV4o0-z5dGdT1u9d5yeXyG9MCrPM</recordid><startdate>20210320</startdate><enddate>20210320</enddate><creator>Wu, Yin</creator><creator>Ding, Ye</creator><creator>Ramprasath, Tharmarajan</creator><creator>Zou, Ming-Hui</creator><general>Mary Ann Liebert, Inc</general><general>Mary Ann Liebert, Inc., publishers</general><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><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>7QL</scope><scope>7QP</scope><scope>7T5</scope><scope>7TK</scope><scope>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-2115-5875</orcidid></search><sort><creationdate>20210320</creationdate><title>Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension</title><author>Wu, Yin ; Ding, Ye ; Ramprasath, Tharmarajan ; Zou, Ming-Hui</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c415t-4d3f56b425fa027f52bbe8b529f58000d6266c8f9c51cb0afad1ca93f9a470c03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Abnormalities</topic><topic>Biochemistry & Molecular Biology</topic><topic>Biopterins - analogs & derivatives</topic><topic>Biopterins - metabolism</topic><topic>Chemical compounds</topic><topic>Clinical trials</topic><topic>Depletion</topic><topic>Endocrinology & Metabolism</topic><topic>Forum Review</topic><topic>GTP Cyclohydrolase - genetics</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Hypertension</topic><topic>Hypertension (Ed. Bin Geng)—Part A</topic><topic>Hypertension - genetics</topic><topic>Hypertension - metabolism</topic><topic>Hypertension - pathology</topic><topic>Information processing</topic><topic>Life Sciences & Biomedicine</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - genetics</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase Type III - genetics</topic><topic>Nitric Oxide Synthase Type III - metabolism</topic><topic>Nitric-oxide synthase</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - genetics</topic><topic>Pharmacology</topic><topic>Regulators</topic><topic>Science & Technology</topic><topic>Signal Transduction - genetics</topic><topic>Signaling</topic><topic>Tetrahydrobiopterin</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Yin</creatorcontrib><creatorcontrib>Ding, Ye</creatorcontrib><creatorcontrib>Ramprasath, Tharmarajan</creatorcontrib><creatorcontrib>Zou, Ming-Hui</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Antioxidants & redox signaling</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Yin</au><au>Ding, Ye</au><au>Ramprasath, Tharmarajan</au><au>Zou, Ming-Hui</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension</atitle><jtitle>Antioxidants & redox signaling</jtitle><stitle>ANTIOXID REDOX SIGN</stitle><addtitle>Antioxid Redox Signal</addtitle><date>2021-03-20</date><risdate>2021</risdate><volume>34</volume><issue>9</issue><spage>750</spage><epage>764</epage><pages>750-764</pages><issn>1523-0864</issn><eissn>1557-7716</eissn><abstract>Significance: Hypertension has major health consequences, which is associated with endothelial dysfunction. Endothelial nitric oxide synthase (eNOS)-produced nitric oxide (NO) signaling in the vasculature plays an important role in maintaining vascular homeostasis. Considering the importance of NO system, this review aims to provide a brief overview of the biochemistry of members of NO signaling, including GTPCH1 [guanosine 5 '-triphosphate (GTP) cyclohydrolase 1], tetrahydrobiopterin (BH4), and eNOS.
Recent Advances: Being NO signaling activators and regulators of eNOS signaling, BH4 treatment is getting widespread attention either as potential therapeutic agents or as preventive agents. Recent clinical trials also support that BH4 treatment could be considered a promising therapeutic in hypertension.
Critical Issues: Under conditions of BH4 depletion, eNOS-generated superoxides trigger pathological events. Abnormalities in NO availability and BH4 deficiency lead to disturbed redox regulation causing pathological events. This disturbed signaling influences the development of systemic hypertension as well as pulmonary hypertension.
Future Directions: Considering the importance of BH4 and NO to improve the translational significance, it is essential to continue research on this field to manipulate BH4 to increase the efficacy for treating hypertension. Thus, this review also examines the current state of knowledge on the effects of eNOS activators on preclinical models and humans to utilize this information for potential therapy.</abstract><cop>NEW ROCHELLE</cop><pub>Mary Ann Liebert, Inc</pub><pmid>32363908</pmid><doi>10.1089/ars.2020.8112</doi><tpages>15</tpages><orcidid>https://orcid.org/0000-0002-2115-5875</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Abnormalities Biochemistry & Molecular Biology Biopterins - analogs & derivatives Biopterins - metabolism Chemical compounds Clinical trials Depletion Endocrinology & Metabolism Forum Review GTP Cyclohydrolase - genetics Homeostasis Humans Hypertension Hypertension (Ed. Bin Geng)—Part A Hypertension - genetics Hypertension - metabolism Hypertension - pathology Information processing Life Sciences & Biomedicine Nitric oxide Nitric Oxide - genetics Nitric Oxide - metabolism Nitric Oxide Synthase Type III - genetics Nitric Oxide Synthase Type III - metabolism Nitric-oxide synthase Oxidative stress Oxidative Stress - genetics Pharmacology Regulators Science & Technology Signal Transduction - genetics Signaling Tetrahydrobiopterin |
| title | Oxidative Stress, GTPCH1, and Endothelial Nitric Oxide Synthase Uncoupling in Hypertension |
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