Crosstalk between mitochondrial (dys)function and mitochondrial abundance

A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed,...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Journal of cellular physiology 2012-06, Vol.227 (6), p.2297-2310
Hauptverfasser: Michel, Sébastien, Wanet, Anaïs, De Pauw, Aurélia, Rommelaere, Guillaume, Arnould, Thierry, Renard, Patricia
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 2310
container_issue 6
container_start_page 2297
container_title Journal of cellular physiology
container_volume 227
creator Michel, Sébastien
Wanet, Anaïs
De Pauw, Aurélia
Rommelaere, Guillaume
Arnould, Thierry
Renard, Patricia
description A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed, with an emphasis on the role of mitochondrial chaperones and proteases that keep mitochondria fully functional, provided the mitochondrial activity impairment is not excessive. In this case, the whole organelle is degraded by mitochondrial autophagy or “mitophagy.” Beside the maintenance of adequate mitochondrial abundance and functions for cell homeostasis, mitochondrial biogenesis might be enhanced, through discussed signaling pathways, in response to various physiological stimuli, like contractile activity, exposure to low temperatures, caloric restriction, and stem cells differentiation. In addition, mitochondrial dysfunction might also initiate a retrograde response, enabling cell adaptation through increased mitochondrial biogenesis. J. Cell. Physiol. 227: 2297–2310, 2012. © 2011 Wiley Periodicals, Inc.
doi_str_mv 10.1002/jcp.23021
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_923955836</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2868530821</sourcerecordid><originalsourceid>FETCH-LOGICAL-c4561-45c9127b757a17c7c02524c5c8b034c5ded02ee0a01d32d75e1f6706764c1dbb3</originalsourceid><addsrcrecordid>eNp1kE1LAzEURYMoWqsL_4AUXGgXoy_JJGmWMtjaUj8QxWXIJClOnWbqZIbaf2-06kJwdRfvvMvlIHSE4RwDkIu5WZ4TCgRvoQ4GKZKUM7KNOvGGE8lSvIf2Q5gDgJSU7qI9giUZ0JR20DirqxAaXb72ctesnPO9RdFU5qXyti502Tuz69Cftd40ReV72ts_d5233mpv3AHamekyuMPv7KKn4dVjdp1M70bj7HKamJRxnKTMSExELpjQWBhhgDCSGmYGOdCY1lkgzoEGbCmxgjk84wK44KnBNs9pF51uepd19da60KhFEYwrS-1d1QYlCZWMDSiP5Mkfcl61tY_jVFwAnFMh00j1N5T5NFG7mVrWxULXa4VBfepVUa_60hvZ4-_GNl84-0v--IzAxQZYFaVb_9-kJtn9T2Wy-ShC495_P3T9qriggqnn25Eacni4GY4makQ_AD2ckgI</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1270663794</pqid></control><display><type>article</type><title>Crosstalk between mitochondrial (dys)function and mitochondrial abundance</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Michel, Sébastien ; Wanet, Anaïs ; De Pauw, Aurélia ; Rommelaere, Guillaume ; Arnould, Thierry ; Renard, Patricia</creator><creatorcontrib>Michel, Sébastien ; Wanet, Anaïs ; De Pauw, Aurélia ; Rommelaere, Guillaume ; Arnould, Thierry ; Renard, Patricia</creatorcontrib><description>A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed, with an emphasis on the role of mitochondrial chaperones and proteases that keep mitochondria fully functional, provided the mitochondrial activity impairment is not excessive. In this case, the whole organelle is degraded by mitochondrial autophagy or “mitophagy.” Beside the maintenance of adequate mitochondrial abundance and functions for cell homeostasis, mitochondrial biogenesis might be enhanced, through discussed signaling pathways, in response to various physiological stimuli, like contractile activity, exposure to low temperatures, caloric restriction, and stem cells differentiation. In addition, mitochondrial dysfunction might also initiate a retrograde response, enabling cell adaptation through increased mitochondrial biogenesis. J. Cell. Physiol. 227: 2297–2310, 2012. © 2011 Wiley Periodicals, Inc.</description><identifier>ISSN: 0021-9541</identifier><identifier>EISSN: 1097-4652</identifier><identifier>DOI: 10.1002/jcp.23021</identifier><identifier>PMID: 21928343</identifier><language>eng</language><publisher>Hoboken: Wiley Subscription Services, Inc., A Wiley Company</publisher><subject>Animals ; Autophagy ; Cellular Senescence ; Dietary restrictions ; DNA Replication ; DNA, Mitochondrial - biosynthesis ; Gene Expression Regulation ; Homeostasis ; Humans ; Low temperature ; Mitochondria - metabolism ; Mitochondria - pathology ; Mitochondrial Proteins - metabolism ; Molecular Chaperones - metabolism ; Peptide Hydrolases - metabolism ; Quality control ; Signal Transduction - genetics ; Stem cells ; Stress, Physiological ; Transcription, Genetic</subject><ispartof>Journal of cellular physiology, 2012-06, Vol.227 (6), p.2297-2310</ispartof><rights>Copyright © 2011 Wiley Periodicals, Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4561-45c9127b757a17c7c02524c5c8b034c5ded02ee0a01d32d75e1f6706764c1dbb3</citedby><cites>FETCH-LOGICAL-c4561-45c9127b757a17c7c02524c5c8b034c5ded02ee0a01d32d75e1f6706764c1dbb3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Fjcp.23021$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Fjcp.23021$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>315,781,785,1418,27926,27927,45576,45577</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21928343$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Michel, Sébastien</creatorcontrib><creatorcontrib>Wanet, Anaïs</creatorcontrib><creatorcontrib>De Pauw, Aurélia</creatorcontrib><creatorcontrib>Rommelaere, Guillaume</creatorcontrib><creatorcontrib>Arnould, Thierry</creatorcontrib><creatorcontrib>Renard, Patricia</creatorcontrib><title>Crosstalk between mitochondrial (dys)function and mitochondrial abundance</title><title>Journal of cellular physiology</title><addtitle>J. Cell. Physiol</addtitle><description>A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed, with an emphasis on the role of mitochondrial chaperones and proteases that keep mitochondria fully functional, provided the mitochondrial activity impairment is not excessive. In this case, the whole organelle is degraded by mitochondrial autophagy or “mitophagy.” Beside the maintenance of adequate mitochondrial abundance and functions for cell homeostasis, mitochondrial biogenesis might be enhanced, through discussed signaling pathways, in response to various physiological stimuli, like contractile activity, exposure to low temperatures, caloric restriction, and stem cells differentiation. In addition, mitochondrial dysfunction might also initiate a retrograde response, enabling cell adaptation through increased mitochondrial biogenesis. J. Cell. Physiol. 227: 2297–2310, 2012. © 2011 Wiley Periodicals, Inc.</description><subject>Animals</subject><subject>Autophagy</subject><subject>Cellular Senescence</subject><subject>Dietary restrictions</subject><subject>DNA Replication</subject><subject>DNA, Mitochondrial - biosynthesis</subject><subject>Gene Expression Regulation</subject><subject>Homeostasis</subject><subject>Humans</subject><subject>Low temperature</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial Proteins - metabolism</subject><subject>Molecular Chaperones - metabolism</subject><subject>Peptide Hydrolases - metabolism</subject><subject>Quality control</subject><subject>Signal Transduction - genetics</subject><subject>Stem cells</subject><subject>Stress, Physiological</subject><subject>Transcription, Genetic</subject><issn>0021-9541</issn><issn>1097-4652</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kE1LAzEURYMoWqsL_4AUXGgXoy_JJGmWMtjaUj8QxWXIJClOnWbqZIbaf2-06kJwdRfvvMvlIHSE4RwDkIu5WZ4TCgRvoQ4GKZKUM7KNOvGGE8lSvIf2Q5gDgJSU7qI9giUZ0JR20DirqxAaXb72ctesnPO9RdFU5qXyti502Tuz69Cftd40ReV72ts_d5233mpv3AHamekyuMPv7KKn4dVjdp1M70bj7HKamJRxnKTMSExELpjQWBhhgDCSGmYGOdCY1lkgzoEGbCmxgjk84wK44KnBNs9pF51uepd19da60KhFEYwrS-1d1QYlCZWMDSiP5Mkfcl61tY_jVFwAnFMh00j1N5T5NFG7mVrWxULXa4VBfepVUa_60hvZ4-_GNl84-0v--IzAxQZYFaVb_9-kJtn9T2Wy-ShC495_P3T9qriggqnn25Eacni4GY4makQ_AD2ckgI</recordid><startdate>201206</startdate><enddate>201206</enddate><creator>Michel, Sébastien</creator><creator>Wanet, Anaïs</creator><creator>De Pauw, Aurélia</creator><creator>Rommelaere, Guillaume</creator><creator>Arnould, Thierry</creator><creator>Renard, Patricia</creator><general>Wiley Subscription Services, Inc., A Wiley Company</general><general>Wiley Subscription Services, Inc</general><scope>BSCLL</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>7TK</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>K9.</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>201206</creationdate><title>Crosstalk between mitochondrial (dys)function and mitochondrial abundance</title><author>Michel, Sébastien ; Wanet, Anaïs ; De Pauw, Aurélia ; Rommelaere, Guillaume ; Arnould, Thierry ; Renard, Patricia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4561-45c9127b757a17c7c02524c5c8b034c5ded02ee0a01d32d75e1f6706764c1dbb3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Autophagy</topic><topic>Cellular Senescence</topic><topic>Dietary restrictions</topic><topic>DNA Replication</topic><topic>DNA, Mitochondrial - biosynthesis</topic><topic>Gene Expression Regulation</topic><topic>Homeostasis</topic><topic>Humans</topic><topic>Low temperature</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>Mitochondrial Proteins - metabolism</topic><topic>Molecular Chaperones - metabolism</topic><topic>Peptide Hydrolases - metabolism</topic><topic>Quality control</topic><topic>Signal Transduction - genetics</topic><topic>Stem cells</topic><topic>Stress, Physiological</topic><topic>Transcription, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Michel, Sébastien</creatorcontrib><creatorcontrib>Wanet, Anaïs</creatorcontrib><creatorcontrib>De Pauw, Aurélia</creatorcontrib><creatorcontrib>Rommelaere, Guillaume</creatorcontrib><creatorcontrib>Arnould, Thierry</creatorcontrib><creatorcontrib>Renard, Patricia</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of cellular physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Michel, Sébastien</au><au>Wanet, Anaïs</au><au>De Pauw, Aurélia</au><au>Rommelaere, Guillaume</au><au>Arnould, Thierry</au><au>Renard, Patricia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Crosstalk between mitochondrial (dys)function and mitochondrial abundance</atitle><jtitle>Journal of cellular physiology</jtitle><addtitle>J. Cell. Physiol</addtitle><date>2012-06</date><risdate>2012</risdate><volume>227</volume><issue>6</issue><spage>2297</spage><epage>2310</epage><pages>2297-2310</pages><issn>0021-9541</issn><eissn>1097-4652</eissn><abstract>A controlled regulation of mitochondrial mass through either the production (biogenesis) or the degradation (mitochondrial quality control) of the organelle represents a crucial step for proper mitochondrial and cell function. Key steps of mitochondrial biogenesis and quality control are overviewed, with an emphasis on the role of mitochondrial chaperones and proteases that keep mitochondria fully functional, provided the mitochondrial activity impairment is not excessive. In this case, the whole organelle is degraded by mitochondrial autophagy or “mitophagy.” Beside the maintenance of adequate mitochondrial abundance and functions for cell homeostasis, mitochondrial biogenesis might be enhanced, through discussed signaling pathways, in response to various physiological stimuli, like contractile activity, exposure to low temperatures, caloric restriction, and stem cells differentiation. In addition, mitochondrial dysfunction might also initiate a retrograde response, enabling cell adaptation through increased mitochondrial biogenesis. J. Cell. Physiol. 227: 2297–2310, 2012. © 2011 Wiley Periodicals, Inc.</abstract><cop>Hoboken</cop><pub>Wiley Subscription Services, Inc., A Wiley Company</pub><pmid>21928343</pmid><doi>10.1002/jcp.23021</doi><tpages>14</tpages></addata></record>
fulltext fulltext
identifier ISSN: 0021-9541
ispartof Journal of cellular physiology, 2012-06, Vol.227 (6), p.2297-2310
issn 0021-9541
1097-4652
language eng
recordid cdi_proquest_miscellaneous_923955836
source MEDLINE; Access via Wiley Online Library
subjects Animals
Autophagy
Cellular Senescence
Dietary restrictions
DNA Replication
DNA, Mitochondrial - biosynthesis
Gene Expression Regulation
Homeostasis
Humans
Low temperature
Mitochondria - metabolism
Mitochondria - pathology
Mitochondrial Proteins - metabolism
Molecular Chaperones - metabolism
Peptide Hydrolases - metabolism
Quality control
Signal Transduction - genetics
Stem cells
Stress, Physiological
Transcription, Genetic
title Crosstalk between mitochondrial (dys)function and mitochondrial abundance
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-18T08%3A03%3A18IST&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=Crosstalk%20between%20mitochondrial%20(dys)function%20and%20mitochondrial%20abundance&rft.jtitle=Journal%20of%20cellular%20physiology&rft.au=Michel,%20S%C3%A9bastien&rft.date=2012-06&rft.volume=227&rft.issue=6&rft.spage=2297&rft.epage=2310&rft.pages=2297-2310&rft.issn=0021-9541&rft.eissn=1097-4652&rft_id=info:doi/10.1002/jcp.23021&rft_dat=%3Cproquest_cross%3E2868530821%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=1270663794&rft_id=info:pmid/21928343&rfr_iscdi=true