EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes: Effect of
Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 ( EEPD1 ) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study, EEPD1 global knockout mice,...
Gespeichert in:
| Veröffentlicht in: | Acta biochimica et biophysica Sinica 2024-08, Vol.56 (12), p.1733-1747 |
|---|---|
| Hauptverfasser: | , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1747 |
|---|---|
| container_issue | 12 |
| container_start_page | 1733 |
| container_title | Acta biochimica et biophysica Sinica |
| container_volume | 56 |
| creator | Yu, Kaiwen Su, Xi Zhou, Tongfang Cai, Xuwei Zhang, Min |
| description | Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 (
EEPD1
) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study,
EEPD1
global knockout mice, C57BL/6J mice, and C57BL/6J mice overexpressing
EEPD1
are treated with radiation at a total dose of 20 Gy or 0 Gy. After 9 weeks, echocardiography is used to assess cardiac hypertrophy and apoptosis. The results show that
EEPD1
deletion exacerbates radiation-induced cardiac hypertrophy and apoptosis, while
EEPD1
overexpression has the opposite effect. Further mechanistic investigations reveal that
EEPD1
interacts with
FOXO3A
and destabilizes it by catalyzing its deubiquitination. Inhibition of
FOXO3A
ameliorates cardiac hypertrophy and apoptosis after
EEPD1
knockdown. Thus,
EEPD1
protects against radiation-induced cardiac hypertrophy and apoptosis via destabilization of
FOXO3A
, which may offer new insight into therapeutic strategies for RIHD. |
| doi_str_mv | 10.3724/abbs.2024130 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmedcentral</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11659772</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>pubmedcentral_primary_oai_pubmedcentral_nih_gov_11659772</sourcerecordid><originalsourceid>FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_116597723</originalsourceid><addsrcrecordid>eNqljLtOwzAYhS0EouWy8QB-gRRfkphMCEEqtjJ06Gb9iU3iqrEt20Hy2xMES2emc3SOvg-hB0o2XLDyEboubhhhJeXkAq2pKKtCMEEul14LVjS0rFboJsYjIbyuKblGK94wSp5YtUbHtv14oxhS0naGpCMOoAwk42xhrJp7rXAPYZl6PGavQwrOjxmDVRi888lFE3GXsdLDD2kHvN0ddvwFG_sLuim7Pi_mO3T1Caeo7__yFj1v2_3re-HnbtKq1zYFOEkfzAQhSwdGnj_WjHJwX5LSumqEYPz_hm-pqmf3</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes: Effect of</title><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><creator>Yu, Kaiwen ; Su, Xi ; Zhou, Tongfang ; Cai, Xuwei ; Zhang, Min</creator><creatorcontrib>Yu, Kaiwen ; Su, Xi ; Zhou, Tongfang ; Cai, Xuwei ; Zhang, Min</creatorcontrib><description>Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 (
EEPD1
) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study,
EEPD1
global knockout mice, C57BL/6J mice, and C57BL/6J mice overexpressing
EEPD1
are treated with radiation at a total dose of 20 Gy or 0 Gy. After 9 weeks, echocardiography is used to assess cardiac hypertrophy and apoptosis. The results show that
EEPD1
deletion exacerbates radiation-induced cardiac hypertrophy and apoptosis, while
EEPD1
overexpression has the opposite effect. Further mechanistic investigations reveal that
EEPD1
interacts with
FOXO3A
and destabilizes it by catalyzing its deubiquitination. Inhibition of
FOXO3A
ameliorates cardiac hypertrophy and apoptosis after
EEPD1
knockdown. Thus,
EEPD1
protects against radiation-induced cardiac hypertrophy and apoptosis via destabilization of
FOXO3A
, which may offer new insight into therapeutic strategies for RIHD.</description><identifier>ISSN: 1672-9145</identifier><identifier>EISSN: 1745-7270</identifier><identifier>DOI: 10.3724/abbs.2024130</identifier><identifier>PMID: 39210825</identifier><language>eng</language><publisher>Science Press</publisher><ispartof>Acta biochimica et biophysica Sinica, 2024-08, Vol.56 (12), p.1733-1747</ispartof><rights>The Author(s) 2021. 2024 The Author(s)</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659772/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC11659772/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27903,27904,53769,53771</link.rule.ids></links><search><creatorcontrib>Yu, Kaiwen</creatorcontrib><creatorcontrib>Su, Xi</creatorcontrib><creatorcontrib>Zhou, Tongfang</creatorcontrib><creatorcontrib>Cai, Xuwei</creatorcontrib><creatorcontrib>Zhang, Min</creatorcontrib><title>EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes: Effect of</title><title>Acta biochimica et biophysica Sinica</title><description>Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 (
EEPD1
) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study,
EEPD1
global knockout mice, C57BL/6J mice, and C57BL/6J mice overexpressing
EEPD1
are treated with radiation at a total dose of 20 Gy or 0 Gy. After 9 weeks, echocardiography is used to assess cardiac hypertrophy and apoptosis. The results show that
EEPD1
deletion exacerbates radiation-induced cardiac hypertrophy and apoptosis, while
EEPD1
overexpression has the opposite effect. Further mechanistic investigations reveal that
EEPD1
interacts with
FOXO3A
and destabilizes it by catalyzing its deubiquitination. Inhibition of
FOXO3A
ameliorates cardiac hypertrophy and apoptosis after
EEPD1
knockdown. Thus,
EEPD1
protects against radiation-induced cardiac hypertrophy and apoptosis via destabilization of
FOXO3A
, which may offer new insight into therapeutic strategies for RIHD.</description><issn>1672-9145</issn><issn>1745-7270</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNqljLtOwzAYhS0EouWy8QB-gRRfkphMCEEqtjJ06Gb9iU3iqrEt20Hy2xMES2emc3SOvg-hB0o2XLDyEboubhhhJeXkAq2pKKtCMEEul14LVjS0rFboJsYjIbyuKblGK94wSp5YtUbHtv14oxhS0naGpCMOoAwk42xhrJp7rXAPYZl6PGavQwrOjxmDVRi888lFE3GXsdLDD2kHvN0ddvwFG_sLuim7Pi_mO3T1Caeo7__yFj1v2_3re-HnbtKq1zYFOEkfzAQhSwdGnj_WjHJwX5LSumqEYPz_hm-pqmf3</recordid><startdate>20240829</startdate><enddate>20240829</enddate><creator>Yu, Kaiwen</creator><creator>Su, Xi</creator><creator>Zhou, Tongfang</creator><creator>Cai, Xuwei</creator><creator>Zhang, Min</creator><general>Science Press</general><scope>5PM</scope></search><sort><creationdate>20240829</creationdate><title>EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes</title><author>Yu, Kaiwen ; Su, Xi ; Zhou, Tongfang ; Cai, Xuwei ; Zhang, Min</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-pubmedcentral_primary_oai_pubmedcentral_nih_gov_116597723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yu, Kaiwen</creatorcontrib><creatorcontrib>Su, Xi</creatorcontrib><creatorcontrib>Zhou, Tongfang</creatorcontrib><creatorcontrib>Cai, Xuwei</creatorcontrib><creatorcontrib>Zhang, Min</creatorcontrib><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta biochimica et biophysica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yu, Kaiwen</au><au>Su, Xi</au><au>Zhou, Tongfang</au><au>Cai, Xuwei</au><au>Zhang, Min</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes: Effect of</atitle><jtitle>Acta biochimica et biophysica Sinica</jtitle><date>2024-08-29</date><risdate>2024</risdate><volume>56</volume><issue>12</issue><spage>1733</spage><epage>1747</epage><pages>1733-1747</pages><issn>1672-9145</issn><eissn>1745-7270</eissn><abstract>Radiation-induced heart disease (RIHD) is a severe delayed complication of thoracic irradiation (IR). Endonuclease/exonuclease/phosphatase family domain-containing 1 (
EEPD1
) plays an important role in DNA damage repair, but its role in RIHD is less known. In this study,
EEPD1
global knockout mice, C57BL/6J mice, and C57BL/6J mice overexpressing
EEPD1
are treated with radiation at a total dose of 20 Gy or 0 Gy. After 9 weeks, echocardiography is used to assess cardiac hypertrophy and apoptosis. The results show that
EEPD1
deletion exacerbates radiation-induced cardiac hypertrophy and apoptosis, while
EEPD1
overexpression has the opposite effect. Further mechanistic investigations reveal that
EEPD1
interacts with
FOXO3A
and destabilizes it by catalyzing its deubiquitination. Inhibition of
FOXO3A
ameliorates cardiac hypertrophy and apoptosis after
EEPD1
knockdown. Thus,
EEPD1
protects against radiation-induced cardiac hypertrophy and apoptosis via destabilization of
FOXO3A
, which may offer new insight into therapeutic strategies for RIHD.</abstract><pub>Science Press</pub><pmid>39210825</pmid><doi>10.3724/abbs.2024130</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1672-9145 |
| ispartof | Acta biochimica et biophysica Sinica, 2024-08, Vol.56 (12), p.1733-1747 |
| issn | 1672-9145 1745-7270 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_11659772 |
| source | DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central |
| title | EEPD1 attenuates radiation-induced cardiac hypertrophy and apoptosis by degrading FOXO3A in cardiomyocytes: Effect of |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-27T23%3A32%3A25IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-pubmedcentral&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=EEPD1%20attenuates%20radiation-induced%20cardiac%20hypertrophy%20and%20apoptosis%20by%20degrading%20FOXO3A%20in%20cardiomyocytes:%20Effect%20of&rft.jtitle=Acta%20biochimica%20et%20biophysica%20Sinica&rft.au=Yu,%20Kaiwen&rft.date=2024-08-29&rft.volume=56&rft.issue=12&rft.spage=1733&rft.epage=1747&rft.pages=1733-1747&rft.issn=1672-9145&rft.eissn=1745-7270&rft_id=info:doi/10.3724/abbs.2024130&rft_dat=%3Cpubmedcentral%3Epubmedcentral_primary_oai_pubmedcentral_nih_gov_11659772%3C/pubmedcentral%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_id=info:pmid/39210825&rfr_iscdi=true |