Purine adducts as a presumable missing link for aristolochic acid nephropathy‐related cellular energy crisis, potential anti‐fibrotic prevention and treatment
Aristolochic acid nephropathy is a progressive exposome‐induced disease characterized by tubular atrophy and fibrosis culminating in end‐stage renal disease and malignancies. The molecular mechanisms of the energy crisis as a putative cause of fibrosis have not yet been elucidated. In light of the f...
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| Veröffentlicht in: | British journal of pharmacology 2021-11, Vol.178 (22), p.4411-4427 |
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| container_title | British journal of pharmacology |
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| creator | Kocic, Gordana Gajic, Mihajlo Tomovic, Katarina Hadzi‐Djokic, Jovan Anderluh, Marko Smelcerovic, Andrija |
| description | Aristolochic acid nephropathy is a progressive exposome‐induced disease characterized by tubular atrophy and fibrosis culminating in end‐stage renal disease and malignancies. The molecular mechanisms of the energy crisis as a putative cause of fibrosis have not yet been elucidated. In light of the fact that aristolochic acid forms DNA and RNA adducts by covalent binding of aristolochic acid metabolites to exocyclic amino groups of (deoxy)adenosine and (deoxy)guanosine, we hypothesize here that similar aristolochic acid adducts may exist with other purine‐containing molecules. We also provide new insights into the aristolochic acid‐induced energy crisis and presumably a link between already known mechanisms. In addition, an overview of potential targets in fibrosis treatment is provided, which is followed by recommendations on possible preventive measures that could be taken to at least postpone or partially alleviate aristolochic acid nephropathy. |
| doi_str_mv | 10.1111/bph.15618 |
| format | Article |
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The molecular mechanisms of the energy crisis as a putative cause of fibrosis have not yet been elucidated. In light of the fact that aristolochic acid forms DNA and RNA adducts by covalent binding of aristolochic acid metabolites to exocyclic amino groups of (deoxy)adenosine and (deoxy)guanosine, we hypothesize here that similar aristolochic acid adducts may exist with other purine‐containing molecules. We also provide new insights into the aristolochic acid‐induced energy crisis and presumably a link between already known mechanisms. In addition, an overview of potential targets in fibrosis treatment is provided, which is followed by recommendations on possible preventive measures that could be taken to at least postpone or partially alleviate aristolochic acid nephropathy.</description><identifier>ISSN: 0007-1188</identifier><identifier>EISSN: 1476-5381</identifier><identifier>DOI: 10.1111/bph.15618</identifier><language>eng</language><publisher>London: Blackwell Publishing Ltd</publisher><subject>Acids ; Adducts ; Adenosine ; Alkalies ; Amino groups ; Aristolochic acid ; aristolochic acid adducts ; aristolochic acid nephropathy ; Atrophy ; DNA adducts ; DPP‐4 ; Energy ; energy crisis ; Energy shortages ; Fibrosis ; Molecular modelling ; Nephropathy</subject><ispartof>British journal of pharmacology, 2021-11, Vol.178 (22), p.4411-4427</ispartof><rights>2021 The British Pharmacological Society</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3988-e18116efb5b73332f9473702c10c3d7b7aff902dd5939597abaeb7f45e5da5393</citedby><cites>FETCH-LOGICAL-c3988-e18116efb5b73332f9473702c10c3d7b7aff902dd5939597abaeb7f45e5da5393</cites><orcidid>0000-0003-1768-8246</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%2Fbph.15618$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fbph.15618$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,1434,27926,27927,45576,45577,46411,46835</link.rule.ids></links><search><creatorcontrib>Kocic, Gordana</creatorcontrib><creatorcontrib>Gajic, Mihajlo</creatorcontrib><creatorcontrib>Tomovic, Katarina</creatorcontrib><creatorcontrib>Hadzi‐Djokic, Jovan</creatorcontrib><creatorcontrib>Anderluh, Marko</creatorcontrib><creatorcontrib>Smelcerovic, Andrija</creatorcontrib><title>Purine adducts as a presumable missing link for aristolochic acid nephropathy‐related cellular energy crisis, potential anti‐fibrotic prevention and treatment</title><title>British journal of pharmacology</title><description>Aristolochic acid nephropathy is a progressive exposome‐induced disease characterized by tubular atrophy and fibrosis culminating in end‐stage renal disease and malignancies. The molecular mechanisms of the energy crisis as a putative cause of fibrosis have not yet been elucidated. In light of the fact that aristolochic acid forms DNA and RNA adducts by covalent binding of aristolochic acid metabolites to exocyclic amino groups of (deoxy)adenosine and (deoxy)guanosine, we hypothesize here that similar aristolochic acid adducts may exist with other purine‐containing molecules. We also provide new insights into the aristolochic acid‐induced energy crisis and presumably a link between already known mechanisms. In addition, an overview of potential targets in fibrosis treatment is provided, which is followed by recommendations on possible preventive measures that could be taken to at least postpone or partially alleviate aristolochic acid nephropathy.</description><subject>Acids</subject><subject>Adducts</subject><subject>Adenosine</subject><subject>Alkalies</subject><subject>Amino groups</subject><subject>Aristolochic acid</subject><subject>aristolochic acid adducts</subject><subject>aristolochic acid nephropathy</subject><subject>Atrophy</subject><subject>DNA adducts</subject><subject>DPP‐4</subject><subject>Energy</subject><subject>energy crisis</subject><subject>Energy shortages</subject><subject>Fibrosis</subject><subject>Molecular modelling</subject><subject>Nephropathy</subject><issn>0007-1188</issn><issn>1476-5381</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><recordid>eNp1kcFOGzEQhi1EJULKgTewxKkSS-x1HO8eadRCJSQ4tOfVrD0mBme92N5WufUR-gx9NJ6kTsOV0Ugjzf_9M4efkHPOrnipRT9urrhc8eaIzPhSrSopGn5MZowxVXHeNCfkNKUnxoqo5Iz8fZiiG5CCMZPOiUJpOkZM0xZ6j3TrUnLDI_VueKY2RArRpRx80BunKWhn6IDjJoYR8mb3-vtPRA8ZDdXo_eQhUhwwPu6oLj6XLukYMg7ZgadQRjFY18eQy7Hy9edeCkORDM0RIW_L4iP5YMEnPHubc_Lj65fv69vq7v7m2_r6rtKibZoKecP5Cm0veyWEqG27VEKxWnOmhVG9AmtbVhsjW9HKVkEP2Cu7lCgNSNGKObk43B1jeJkw5e4pTHEoL7taNrLmatnyQn06UDqGlCLaboxuC3HXcdbtI-hKBN3_CAq7OLC_nMfd-2D3-eH24PgHhXqOZg</recordid><startdate>202111</startdate><enddate>202111</enddate><creator>Kocic, Gordana</creator><creator>Gajic, Mihajlo</creator><creator>Tomovic, Katarina</creator><creator>Hadzi‐Djokic, Jovan</creator><creator>Anderluh, Marko</creator><creator>Smelcerovic, Andrija</creator><general>Blackwell Publishing Ltd</general><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7TK</scope><scope>K9.</scope><scope>NAPCQ</scope><orcidid>https://orcid.org/0000-0003-1768-8246</orcidid></search><sort><creationdate>202111</creationdate><title>Purine adducts as a presumable missing link for aristolochic acid nephropathy‐related cellular energy crisis, potential anti‐fibrotic prevention and treatment</title><author>Kocic, Gordana ; Gajic, Mihajlo ; Tomovic, Katarina ; Hadzi‐Djokic, Jovan ; Anderluh, Marko ; Smelcerovic, Andrija</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3988-e18116efb5b73332f9473702c10c3d7b7aff902dd5939597abaeb7f45e5da5393</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Acids</topic><topic>Adducts</topic><topic>Adenosine</topic><topic>Alkalies</topic><topic>Amino groups</topic><topic>Aristolochic acid</topic><topic>aristolochic acid adducts</topic><topic>aristolochic acid nephropathy</topic><topic>Atrophy</topic><topic>DNA adducts</topic><topic>DPP‐4</topic><topic>Energy</topic><topic>energy crisis</topic><topic>Energy shortages</topic><topic>Fibrosis</topic><topic>Molecular modelling</topic><topic>Nephropathy</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kocic, Gordana</creatorcontrib><creatorcontrib>Gajic, Mihajlo</creatorcontrib><creatorcontrib>Tomovic, Katarina</creatorcontrib><creatorcontrib>Hadzi‐Djokic, Jovan</creatorcontrib><creatorcontrib>Anderluh, Marko</creatorcontrib><creatorcontrib>Smelcerovic, Andrija</creatorcontrib><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>British journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kocic, Gordana</au><au>Gajic, Mihajlo</au><au>Tomovic, Katarina</au><au>Hadzi‐Djokic, Jovan</au><au>Anderluh, Marko</au><au>Smelcerovic, Andrija</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Purine adducts as a presumable missing link for aristolochic acid nephropathy‐related cellular energy crisis, potential anti‐fibrotic prevention and treatment</atitle><jtitle>British journal of pharmacology</jtitle><date>2021-11</date><risdate>2021</risdate><volume>178</volume><issue>22</issue><spage>4411</spage><epage>4427</epage><pages>4411-4427</pages><issn>0007-1188</issn><eissn>1476-5381</eissn><abstract>Aristolochic acid nephropathy is a progressive exposome‐induced disease characterized by tubular atrophy and fibrosis culminating in end‐stage renal disease and malignancies. 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| subjects | Acids Adducts Adenosine Alkalies Amino groups Aristolochic acid aristolochic acid adducts aristolochic acid nephropathy Atrophy DNA adducts DPP‐4 Energy energy crisis Energy shortages Fibrosis Molecular modelling Nephropathy |
| title | Purine adducts as a presumable missing link for aristolochic acid nephropathy‐related cellular energy crisis, potential anti‐fibrotic prevention and treatment |
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