A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury

Apoptosis repressor with caspase recruitment domain (ARC) acts as a potent and multifunctional inhibitor of apoptosis, which is mainly expressed in postmitotic cells, including cardiomyocytes. ARC is special for its N-terminal caspase recruitment domain and caspase recruitment domain. Due to the pow...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Apoptosis (London) 2023-04, Vol.28 (3-4), p.313-325
Hauptverfasser: Liu, Kun, Lan, Dongfeng, Li, Chunyang, Liu, Songpo, Dai, Xiaofang, Song, Tao, Wang, Xianyao, Kong, Qinghong, He, Zhixu, Tan, Jun, Zhang, Jidong
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 325
container_issue 3-4
container_start_page 313
container_title Apoptosis (London)
container_volume 28
creator Liu, Kun
Lan, Dongfeng
Li, Chunyang
Liu, Songpo
Dai, Xiaofang
Song, Tao
Wang, Xianyao
Kong, Qinghong
He, Zhixu
Tan, Jun
Zhang, Jidong
description Apoptosis repressor with caspase recruitment domain (ARC) acts as a potent and multifunctional inhibitor of apoptosis, which is mainly expressed in postmitotic cells, including cardiomyocytes. ARC is special for its N-terminal caspase recruitment domain and caspase recruitment domain. Due to the powerful inhibition of apoptosis, ARC is mainly reported to act as a cardioprotective factor during ischaemia‒reperfusion (I/R) injury, preventing cardiomyocytes from being devastated by various catastrophes, including oxidative stress, calcium overload, and mitochondrial dysfunction in the circulatory system. However, recent studies have found that ARC also plays a potential regulatory role in tumorigenesis especially in colorectal cancer and renal cell carcinomas, through multiple apoptosis-associated pathways, which remains to be explored in further studies. Therefore, ARC regulates the body and maintains the balance of physiological activities with its interesting duplex. This review summarizes the current research progress of ARC in the field of tumorigenesis and ischaemia/reperfusion injury, to provide overall research status and new possibilities for researchers.
doi_str_mv 10.1007/s10495-022-01802-4
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_2766721089</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2766721089</sourcerecordid><originalsourceid>FETCH-LOGICAL-c375t-2b39fe658d47346cf47e277bfe7db06df8fa5e1b4e92a6fc7f7f82b5e1e9fd643</originalsourceid><addsrcrecordid>eNp9kc2KFDEUhYMozjj6Ai4k4GZcxM5fJVXumsafgQFhUHAXUpWbnjRVlTKpMMxT-Mqm7VHBhatcbs75cshB6CWjbxmlepMZlV1DKOeEspZyIh-hc9ZoQZRuvj2us1CUtKxtztCznA-UUtEK-RSdCaUaznh7jn5ssYulH4GA24PD-S4m9w6nOAKOHtslLmvMIeMES4KcY8J3Yb3Fg82LzVDXQyphnWBeK2iyYcaX25vdG1yHtUwxhT3McATY2eGQh1sLU7CbioPkSw6xGq42N0fDoaT75-iJt2OGFw_nBfr64f2X3Sdy_fnj1W57TQahm5XwXnQeVNM6qYVUg5cauNa9B-16qpxvvW2A9RI6bpUftNe-5X1dQeedkuICXZ64S4rfC-TVTDUcjKOdIZZsuFZKc0bbrkpf_yM9xJLmms7w-utKSi1ZVfGTakgx5wTeLClMNt0bRs2xLnOqy9S6zK-6zDHFqwd06Sdwfyy_-6kCcRLkejXvIf19-z_Yn-IwoiA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2802644741</pqid></control><display><type>article</type><title>A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Liu, Kun ; Lan, Dongfeng ; Li, Chunyang ; Liu, Songpo ; Dai, Xiaofang ; Song, Tao ; Wang, Xianyao ; Kong, Qinghong ; He, Zhixu ; Tan, Jun ; Zhang, Jidong</creator><creatorcontrib>Liu, Kun ; Lan, Dongfeng ; Li, Chunyang ; Liu, Songpo ; Dai, Xiaofang ; Song, Tao ; Wang, Xianyao ; Kong, Qinghong ; He, Zhixu ; Tan, Jun ; Zhang, Jidong</creatorcontrib><description>Apoptosis repressor with caspase recruitment domain (ARC) acts as a potent and multifunctional inhibitor of apoptosis, which is mainly expressed in postmitotic cells, including cardiomyocytes. ARC is special for its N-terminal caspase recruitment domain and caspase recruitment domain. Due to the powerful inhibition of apoptosis, ARC is mainly reported to act as a cardioprotective factor during ischaemia‒reperfusion (I/R) injury, preventing cardiomyocytes from being devastated by various catastrophes, including oxidative stress, calcium overload, and mitochondrial dysfunction in the circulatory system. However, recent studies have found that ARC also plays a potential regulatory role in tumorigenesis especially in colorectal cancer and renal cell carcinomas, through multiple apoptosis-associated pathways, which remains to be explored in further studies. Therefore, ARC regulates the body and maintains the balance of physiological activities with its interesting duplex. This review summarizes the current research progress of ARC in the field of tumorigenesis and ischaemia/reperfusion injury, to provide overall research status and new possibilities for researchers.</description><identifier>ISSN: 1360-8185</identifier><identifier>EISSN: 1573-675X</identifier><identifier>DOI: 10.1007/s10495-022-01802-4</identifier><identifier>PMID: 36652128</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Apoptosis - genetics ; Apoptosis Regulatory Proteins - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Calcium (mitochondrial) ; Cancer ; Cancer Research ; Carcinogenesis - genetics ; Cardiomyocytes ; Caspase ; Caspase Activation and Recruitment Domain ; Cell Biology ; Cell Transformation, Neoplastic ; Circulatory system ; Colorectal carcinoma ; Disasters ; Domains ; Humans ; Injury prevention ; Ischemia ; Kidney cancer ; Mitochondria ; Oncology ; Oxidative stress ; Recruitment ; Renal cell carcinoma ; Reperfusion ; Reperfusion Injury - genetics ; Review ; Tumorigenesis ; Virology</subject><ispartof>Apoptosis (London), 2023-04, Vol.28 (3-4), p.313-325</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-2b39fe658d47346cf47e277bfe7db06df8fa5e1b4e92a6fc7f7f82b5e1e9fd643</citedby><cites>FETCH-LOGICAL-c375t-2b39fe658d47346cf47e277bfe7db06df8fa5e1b4e92a6fc7f7f82b5e1e9fd643</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10495-022-01802-4$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10495-022-01802-4$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/36652128$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Kun</creatorcontrib><creatorcontrib>Lan, Dongfeng</creatorcontrib><creatorcontrib>Li, Chunyang</creatorcontrib><creatorcontrib>Liu, Songpo</creatorcontrib><creatorcontrib>Dai, Xiaofang</creatorcontrib><creatorcontrib>Song, Tao</creatorcontrib><creatorcontrib>Wang, Xianyao</creatorcontrib><creatorcontrib>Kong, Qinghong</creatorcontrib><creatorcontrib>He, Zhixu</creatorcontrib><creatorcontrib>Tan, Jun</creatorcontrib><creatorcontrib>Zhang, Jidong</creatorcontrib><title>A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury</title><title>Apoptosis (London)</title><addtitle>Apoptosis</addtitle><addtitle>Apoptosis</addtitle><description>Apoptosis repressor with caspase recruitment domain (ARC) acts as a potent and multifunctional inhibitor of apoptosis, which is mainly expressed in postmitotic cells, including cardiomyocytes. ARC is special for its N-terminal caspase recruitment domain and caspase recruitment domain. Due to the powerful inhibition of apoptosis, ARC is mainly reported to act as a cardioprotective factor during ischaemia‒reperfusion (I/R) injury, preventing cardiomyocytes from being devastated by various catastrophes, including oxidative stress, calcium overload, and mitochondrial dysfunction in the circulatory system. However, recent studies have found that ARC also plays a potential regulatory role in tumorigenesis especially in colorectal cancer and renal cell carcinomas, through multiple apoptosis-associated pathways, which remains to be explored in further studies. Therefore, ARC regulates the body and maintains the balance of physiological activities with its interesting duplex. This review summarizes the current research progress of ARC in the field of tumorigenesis and ischaemia/reperfusion injury, to provide overall research status and new possibilities for researchers.</description><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Calcium (mitochondrial)</subject><subject>Cancer</subject><subject>Cancer Research</subject><subject>Carcinogenesis - genetics</subject><subject>Cardiomyocytes</subject><subject>Caspase</subject><subject>Caspase Activation and Recruitment Domain</subject><subject>Cell Biology</subject><subject>Cell Transformation, Neoplastic</subject><subject>Circulatory system</subject><subject>Colorectal carcinoma</subject><subject>Disasters</subject><subject>Domains</subject><subject>Humans</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>Kidney cancer</subject><subject>Mitochondria</subject><subject>Oncology</subject><subject>Oxidative stress</subject><subject>Recruitment</subject><subject>Renal cell carcinoma</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - genetics</subject><subject>Review</subject><subject>Tumorigenesis</subject><subject>Virology</subject><issn>1360-8185</issn><issn>1573-675X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc2KFDEUhYMozjj6Ai4k4GZcxM5fJVXumsafgQFhUHAXUpWbnjRVlTKpMMxT-Mqm7VHBhatcbs75cshB6CWjbxmlepMZlV1DKOeEspZyIh-hc9ZoQZRuvj2us1CUtKxtztCznA-UUtEK-RSdCaUaznh7jn5ssYulH4GA24PD-S4m9w6nOAKOHtslLmvMIeMES4KcY8J3Yb3Fg82LzVDXQyphnWBeK2iyYcaX25vdG1yHtUwxhT3McATY2eGQh1sLU7CbioPkSw6xGq42N0fDoaT75-iJt2OGFw_nBfr64f2X3Sdy_fnj1W57TQahm5XwXnQeVNM6qYVUg5cauNa9B-16qpxvvW2A9RI6bpUftNe-5X1dQeedkuICXZ64S4rfC-TVTDUcjKOdIZZsuFZKc0bbrkpf_yM9xJLmms7w-utKSi1ZVfGTakgx5wTeLClMNt0bRs2xLnOqy9S6zK-6zDHFqwd06Sdwfyy_-6kCcRLkejXvIf19-z_Yn-IwoiA</recordid><startdate>20230401</startdate><enddate>20230401</enddate><creator>Liu, Kun</creator><creator>Lan, Dongfeng</creator><creator>Li, Chunyang</creator><creator>Liu, Songpo</creator><creator>Dai, Xiaofang</creator><creator>Song, Tao</creator><creator>Wang, Xianyao</creator><creator>Kong, Qinghong</creator><creator>He, Zhixu</creator><creator>Tan, Jun</creator><creator>Zhang, Jidong</creator><general>Springer US</general><general>Springer Nature B.V</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>3V.</scope><scope>7QL</scope><scope>7QP</scope><scope>7RQ</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20230401</creationdate><title>A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury</title><author>Liu, Kun ; Lan, Dongfeng ; Li, Chunyang ; Liu, Songpo ; Dai, Xiaofang ; Song, Tao ; Wang, Xianyao ; Kong, Qinghong ; He, Zhixu ; Tan, Jun ; Zhang, Jidong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-2b39fe658d47346cf47e277bfe7db06df8fa5e1b4e92a6fc7f7f82b5e1e9fd643</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Calcium (mitochondrial)</topic><topic>Cancer</topic><topic>Cancer Research</topic><topic>Carcinogenesis - genetics</topic><topic>Cardiomyocytes</topic><topic>Caspase</topic><topic>Caspase Activation and Recruitment Domain</topic><topic>Cell Biology</topic><topic>Cell Transformation, Neoplastic</topic><topic>Circulatory system</topic><topic>Colorectal carcinoma</topic><topic>Disasters</topic><topic>Domains</topic><topic>Humans</topic><topic>Injury prevention</topic><topic>Ischemia</topic><topic>Kidney cancer</topic><topic>Mitochondria</topic><topic>Oncology</topic><topic>Oxidative stress</topic><topic>Recruitment</topic><topic>Renal cell carcinoma</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - genetics</topic><topic>Review</topic><topic>Tumorigenesis</topic><topic>Virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Kun</creatorcontrib><creatorcontrib>Lan, Dongfeng</creatorcontrib><creatorcontrib>Li, Chunyang</creatorcontrib><creatorcontrib>Liu, Songpo</creatorcontrib><creatorcontrib>Dai, Xiaofang</creatorcontrib><creatorcontrib>Song, Tao</creatorcontrib><creatorcontrib>Wang, Xianyao</creatorcontrib><creatorcontrib>Kong, Qinghong</creatorcontrib><creatorcontrib>He, Zhixu</creatorcontrib><creatorcontrib>Tan, Jun</creatorcontrib><creatorcontrib>Zhang, Jidong</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Career &amp; Technical Education Database</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>ProQuest Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Apoptosis (London)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Kun</au><au>Lan, Dongfeng</au><au>Li, Chunyang</au><au>Liu, Songpo</au><au>Dai, Xiaofang</au><au>Song, Tao</au><au>Wang, Xianyao</au><au>Kong, Qinghong</au><au>He, Zhixu</au><au>Tan, Jun</au><au>Zhang, Jidong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury</atitle><jtitle>Apoptosis (London)</jtitle><stitle>Apoptosis</stitle><addtitle>Apoptosis</addtitle><date>2023-04-01</date><risdate>2023</risdate><volume>28</volume><issue>3-4</issue><spage>313</spage><epage>325</epage><pages>313-325</pages><issn>1360-8185</issn><eissn>1573-675X</eissn><abstract>Apoptosis repressor with caspase recruitment domain (ARC) acts as a potent and multifunctional inhibitor of apoptosis, which is mainly expressed in postmitotic cells, including cardiomyocytes. ARC is special for its N-terminal caspase recruitment domain and caspase recruitment domain. Due to the powerful inhibition of apoptosis, ARC is mainly reported to act as a cardioprotective factor during ischaemia‒reperfusion (I/R) injury, preventing cardiomyocytes from being devastated by various catastrophes, including oxidative stress, calcium overload, and mitochondrial dysfunction in the circulatory system. However, recent studies have found that ARC also plays a potential regulatory role in tumorigenesis especially in colorectal cancer and renal cell carcinomas, through multiple apoptosis-associated pathways, which remains to be explored in further studies. Therefore, ARC regulates the body and maintains the balance of physiological activities with its interesting duplex. This review summarizes the current research progress of ARC in the field of tumorigenesis and ischaemia/reperfusion injury, to provide overall research status and new possibilities for researchers.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36652128</pmid><doi>10.1007/s10495-022-01802-4</doi><tpages>13</tpages></addata></record>
fulltext fulltext
identifier ISSN: 1360-8185
ispartof Apoptosis (London), 2023-04, Vol.28 (3-4), p.313-325
issn 1360-8185
1573-675X
language eng
recordid cdi_proquest_miscellaneous_2766721089
source MEDLINE; SpringerLink Journals - AutoHoldings
subjects Apoptosis
Apoptosis - genetics
Apoptosis Regulatory Proteins - metabolism
Biochemistry
Biomedical and Life Sciences
Biomedicine
Calcium (mitochondrial)
Cancer
Cancer Research
Carcinogenesis - genetics
Cardiomyocytes
Caspase
Caspase Activation and Recruitment Domain
Cell Biology
Cell Transformation, Neoplastic
Circulatory system
Colorectal carcinoma
Disasters
Domains
Humans
Injury prevention
Ischemia
Kidney cancer
Mitochondria
Oncology
Oxidative stress
Recruitment
Renal cell carcinoma
Reperfusion
Reperfusion Injury - genetics
Review
Tumorigenesis
Virology
title A double-edged sword: role of apoptosis repressor with caspase recruitment domain (ARC) in tumorigenesis and ischaemia/reperfusion (I/R) injury
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-10T15%3A51%3A04IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=A%20double-edged%20sword:%20role%20of%20apoptosis%20repressor%20with%20caspase%20recruitment%20domain%20(ARC)%20in%20tumorigenesis%20and%20ischaemia/reperfusion%20(I/R)%20injury&rft.jtitle=Apoptosis%20(London)&rft.au=Liu,%20Kun&rft.date=2023-04-01&rft.volume=28&rft.issue=3-4&rft.spage=313&rft.epage=325&rft.pages=313-325&rft.issn=1360-8185&rft.eissn=1573-675X&rft_id=info:doi/10.1007/s10495-022-01802-4&rft_dat=%3Cproquest_cross%3E2766721089%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2802644741&rft_id=info:pmid/36652128&rfr_iscdi=true