Egr1 regulates regenerative senescence and cardiac repair
Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cel...
Gespeichert in:
| Veröffentlicht in: | Nature Cardiovascular Research 2024-08, Vol.3 (8), p.915-932 |
|---|---|
| Hauptverfasser: | , , , , , , , , , , , , , , , , , , , , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 932 |
|---|---|
| container_issue | 8 |
| container_start_page | 915 |
| container_title | Nature Cardiovascular Research |
| container_volume | 3 |
| creator | Zhang, Lingling Elkahal, Jacob Wang, Tianzhen Rimmer, Racheli Genzelinakh, Alexander Bassat, Elad Wang, Jingkui Perez, Dahlia Kain, David Lendengolts, Daria Winkler, Roni Bueno-Levy, Hanna Umansky, Kfir Baruch Mishaly, David Shakked, Avraham Miyara, Shoval Sarusi-Portuguez, Avital Goldfinger, Naomi Prior, Amir Morgenstern, David Levin, Yishai Addadi, Yoseph Li, Baoguo Rotter, Varda Katz, Uriel Tanaka, Elly M Krizhanovsky, Valery Sarig, Rachel Tzahor, Eldad |
| description | Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, agrin-induced senescence and repair require Egr1, activated by the integrin-FAK-ERK-Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype components that promote extracellular matrix degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process. |
| doi_str_mv | 10.1038/s44161-024-00493-1 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_3097855533</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>3097855533</sourcerecordid><originalsourceid>FETCH-LOGICAL-c254t-36ed8fe822a7f72adee6a7e34a64529cfc5c8a19b42531facff38a1d77998c363</originalsourceid><addsrcrecordid>eNpNkE9LAzEQxYMottR-AQ-yRy-rSSbZbI5S6h8oeNFzmGYnZWG7rcmu4Lc3tVU8zZvhvcfwY-xa8DvBob5PSolKlFyqknNloRRnbCoN5JO2_PyfnrB5Su2aq0rW2oC5ZBOwwlZcmimzy00URaTN2OFA6aCop4hD-0lFyjJ56j0V2DeFx9i06LNnj228YhcBu0Tz05yx98fl2-K5XL0-vSweVqWXWg0lVNTUgWop0QQjsSGq0BAorJSW1gevfY3CrpXUIAL6ECDvjTHW1h4qmLHbY-8-7j5GSoPbtvmprsOedmNywK2ptdYA2SqPVh93KUUKbh_bLcYvJ7g7UHNHai5Tcz_UnMihm1P_uN5S8xf5ZQTfFiBnfQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>3097855533</pqid></control><display><type>article</type><title>Egr1 regulates regenerative senescence and cardiac repair</title><source>MEDLINE</source><source>Springer Nature - Complete Springer Journals</source><creator>Zhang, Lingling ; Elkahal, Jacob ; Wang, Tianzhen ; Rimmer, Racheli ; Genzelinakh, Alexander ; Bassat, Elad ; Wang, Jingkui ; Perez, Dahlia ; Kain, David ; Lendengolts, Daria ; Winkler, Roni ; Bueno-Levy, Hanna ; Umansky, Kfir Baruch ; Mishaly, David ; Shakked, Avraham ; Miyara, Shoval ; Sarusi-Portuguez, Avital ; Goldfinger, Naomi ; Prior, Amir ; Morgenstern, David ; Levin, Yishai ; Addadi, Yoseph ; Li, Baoguo ; Rotter, Varda ; Katz, Uriel ; Tanaka, Elly M ; Krizhanovsky, Valery ; Sarig, Rachel ; Tzahor, Eldad</creator><creatorcontrib>Zhang, Lingling ; Elkahal, Jacob ; Wang, Tianzhen ; Rimmer, Racheli ; Genzelinakh, Alexander ; Bassat, Elad ; Wang, Jingkui ; Perez, Dahlia ; Kain, David ; Lendengolts, Daria ; Winkler, Roni ; Bueno-Levy, Hanna ; Umansky, Kfir Baruch ; Mishaly, David ; Shakked, Avraham ; Miyara, Shoval ; Sarusi-Portuguez, Avital ; Goldfinger, Naomi ; Prior, Amir ; Morgenstern, David ; Levin, Yishai ; Addadi, Yoseph ; Li, Baoguo ; Rotter, Varda ; Katz, Uriel ; Tanaka, Elly M ; Krizhanovsky, Valery ; Sarig, Rachel ; Tzahor, Eldad</creatorcontrib><description>Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, agrin-induced senescence and repair require Egr1, activated by the integrin-FAK-ERK-Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype components that promote extracellular matrix degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process.</description><identifier>ISSN: 2731-0590</identifier><identifier>EISSN: 2731-0590</identifier><identifier>DOI: 10.1038/s44161-024-00493-1</identifier><identifier>PMID: 39196027</identifier><language>eng</language><publisher>England</publisher><subject>Animals ; Animals, Newborn ; Cell Proliferation ; Cells, Cultured ; Cellular Senescence - physiology ; Disease Models, Animal ; Early Growth Response Protein 1 - genetics ; Early Growth Response Protein 1 - metabolism ; Extracellular Signal-Regulated MAP Kinases - metabolism ; Fibroblasts - metabolism ; Focal Adhesion Kinase 1 ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Myocytes, Cardiac - metabolism ; Neovascularization, Physiologic - physiology ; Proteomics ; Proto-Oncogene Proteins c-akt - metabolism ; Regeneration - physiology ; Senescence-Associated Secretory Phenotype ; Signal Transduction ; Single-Cell Analysis</subject><ispartof>Nature Cardiovascular Research, 2024-08, Vol.3 (8), p.915-932</ispartof><rights>2024. The Author(s), under exclusive licence to Springer Nature Limited.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c254t-36ed8fe822a7f72adee6a7e34a64529cfc5c8a19b42531facff38a1d77998c363</cites><orcidid>0000-0002-0628-1443 ; 0000-0003-0157-7162 ; 0000-0002-9003-046X ; 0000-0002-5212-9426 ; 0000-0001-9827-0436 ; 0000-0003-4240-2158 ; 0000-0003-0541-3069 ; 0000-0002-4132-5114</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/39196027$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhang, Lingling</creatorcontrib><creatorcontrib>Elkahal, Jacob</creatorcontrib><creatorcontrib>Wang, Tianzhen</creatorcontrib><creatorcontrib>Rimmer, Racheli</creatorcontrib><creatorcontrib>Genzelinakh, Alexander</creatorcontrib><creatorcontrib>Bassat, Elad</creatorcontrib><creatorcontrib>Wang, Jingkui</creatorcontrib><creatorcontrib>Perez, Dahlia</creatorcontrib><creatorcontrib>Kain, David</creatorcontrib><creatorcontrib>Lendengolts, Daria</creatorcontrib><creatorcontrib>Winkler, Roni</creatorcontrib><creatorcontrib>Bueno-Levy, Hanna</creatorcontrib><creatorcontrib>Umansky, Kfir Baruch</creatorcontrib><creatorcontrib>Mishaly, David</creatorcontrib><creatorcontrib>Shakked, Avraham</creatorcontrib><creatorcontrib>Miyara, Shoval</creatorcontrib><creatorcontrib>Sarusi-Portuguez, Avital</creatorcontrib><creatorcontrib>Goldfinger, Naomi</creatorcontrib><creatorcontrib>Prior, Amir</creatorcontrib><creatorcontrib>Morgenstern, David</creatorcontrib><creatorcontrib>Levin, Yishai</creatorcontrib><creatorcontrib>Addadi, Yoseph</creatorcontrib><creatorcontrib>Li, Baoguo</creatorcontrib><creatorcontrib>Rotter, Varda</creatorcontrib><creatorcontrib>Katz, Uriel</creatorcontrib><creatorcontrib>Tanaka, Elly M</creatorcontrib><creatorcontrib>Krizhanovsky, Valery</creatorcontrib><creatorcontrib>Sarig, Rachel</creatorcontrib><creatorcontrib>Tzahor, Eldad</creatorcontrib><title>Egr1 regulates regenerative senescence and cardiac repair</title><title>Nature Cardiovascular Research</title><addtitle>Nat Cardiovasc Res</addtitle><description>Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, agrin-induced senescence and repair require Egr1, activated by the integrin-FAK-ERK-Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype components that promote extracellular matrix degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process.</description><subject>Animals</subject><subject>Animals, Newborn</subject><subject>Cell Proliferation</subject><subject>Cells, Cultured</subject><subject>Cellular Senescence - physiology</subject><subject>Disease Models, Animal</subject><subject>Early Growth Response Protein 1 - genetics</subject><subject>Early Growth Response Protein 1 - metabolism</subject><subject>Extracellular Signal-Regulated MAP Kinases - metabolism</subject><subject>Fibroblasts - metabolism</subject><subject>Focal Adhesion Kinase 1</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Proteomics</subject><subject>Proto-Oncogene Proteins c-akt - metabolism</subject><subject>Regeneration - physiology</subject><subject>Senescence-Associated Secretory Phenotype</subject><subject>Signal Transduction</subject><subject>Single-Cell Analysis</subject><issn>2731-0590</issn><issn>2731-0590</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkE9LAzEQxYMottR-AQ-yRy-rSSbZbI5S6h8oeNFzmGYnZWG7rcmu4Lc3tVU8zZvhvcfwY-xa8DvBob5PSolKlFyqknNloRRnbCoN5JO2_PyfnrB5Su2aq0rW2oC5ZBOwwlZcmimzy00URaTN2OFA6aCop4hD-0lFyjJ56j0V2DeFx9i06LNnj228YhcBu0Tz05yx98fl2-K5XL0-vSweVqWXWg0lVNTUgWop0QQjsSGq0BAorJSW1gevfY3CrpXUIAL6ECDvjTHW1h4qmLHbY-8-7j5GSoPbtvmprsOedmNywK2ptdYA2SqPVh93KUUKbh_bLcYvJ7g7UHNHai5Tcz_UnMihm1P_uN5S8xf5ZQTfFiBnfQ</recordid><startdate>20240801</startdate><enddate>20240801</enddate><creator>Zhang, Lingling</creator><creator>Elkahal, Jacob</creator><creator>Wang, Tianzhen</creator><creator>Rimmer, Racheli</creator><creator>Genzelinakh, Alexander</creator><creator>Bassat, Elad</creator><creator>Wang, Jingkui</creator><creator>Perez, Dahlia</creator><creator>Kain, David</creator><creator>Lendengolts, Daria</creator><creator>Winkler, Roni</creator><creator>Bueno-Levy, Hanna</creator><creator>Umansky, Kfir Baruch</creator><creator>Mishaly, David</creator><creator>Shakked, Avraham</creator><creator>Miyara, Shoval</creator><creator>Sarusi-Portuguez, Avital</creator><creator>Goldfinger, Naomi</creator><creator>Prior, Amir</creator><creator>Morgenstern, David</creator><creator>Levin, Yishai</creator><creator>Addadi, Yoseph</creator><creator>Li, Baoguo</creator><creator>Rotter, Varda</creator><creator>Katz, Uriel</creator><creator>Tanaka, Elly M</creator><creator>Krizhanovsky, Valery</creator><creator>Sarig, Rachel</creator><creator>Tzahor, Eldad</creator><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>7X8</scope><orcidid>https://orcid.org/0000-0002-0628-1443</orcidid><orcidid>https://orcid.org/0000-0003-0157-7162</orcidid><orcidid>https://orcid.org/0000-0002-9003-046X</orcidid><orcidid>https://orcid.org/0000-0002-5212-9426</orcidid><orcidid>https://orcid.org/0000-0001-9827-0436</orcidid><orcidid>https://orcid.org/0000-0003-4240-2158</orcidid><orcidid>https://orcid.org/0000-0003-0541-3069</orcidid><orcidid>https://orcid.org/0000-0002-4132-5114</orcidid></search><sort><creationdate>20240801</creationdate><title>Egr1 regulates regenerative senescence and cardiac repair</title><author>Zhang, Lingling ; Elkahal, Jacob ; Wang, Tianzhen ; Rimmer, Racheli ; Genzelinakh, Alexander ; Bassat, Elad ; Wang, Jingkui ; Perez, Dahlia ; Kain, David ; Lendengolts, Daria ; Winkler, Roni ; Bueno-Levy, Hanna ; Umansky, Kfir Baruch ; Mishaly, David ; Shakked, Avraham ; Miyara, Shoval ; Sarusi-Portuguez, Avital ; Goldfinger, Naomi ; Prior, Amir ; Morgenstern, David ; Levin, Yishai ; Addadi, Yoseph ; Li, Baoguo ; Rotter, Varda ; Katz, Uriel ; Tanaka, Elly M ; Krizhanovsky, Valery ; Sarig, Rachel ; Tzahor, Eldad</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c254t-36ed8fe822a7f72adee6a7e34a64529cfc5c8a19b42531facff38a1d77998c363</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Animals, Newborn</topic><topic>Cell Proliferation</topic><topic>Cells, Cultured</topic><topic>Cellular Senescence - physiology</topic><topic>Disease Models, Animal</topic><topic>Early Growth Response Protein 1 - genetics</topic><topic>Early Growth Response Protein 1 - metabolism</topic><topic>Extracellular Signal-Regulated MAP Kinases - metabolism</topic><topic>Fibroblasts - metabolism</topic><topic>Focal Adhesion Kinase 1</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Proteomics</topic><topic>Proto-Oncogene Proteins c-akt - metabolism</topic><topic>Regeneration - physiology</topic><topic>Senescence-Associated Secretory Phenotype</topic><topic>Signal Transduction</topic><topic>Single-Cell Analysis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhang, Lingling</creatorcontrib><creatorcontrib>Elkahal, Jacob</creatorcontrib><creatorcontrib>Wang, Tianzhen</creatorcontrib><creatorcontrib>Rimmer, Racheli</creatorcontrib><creatorcontrib>Genzelinakh, Alexander</creatorcontrib><creatorcontrib>Bassat, Elad</creatorcontrib><creatorcontrib>Wang, Jingkui</creatorcontrib><creatorcontrib>Perez, Dahlia</creatorcontrib><creatorcontrib>Kain, David</creatorcontrib><creatorcontrib>Lendengolts, Daria</creatorcontrib><creatorcontrib>Winkler, Roni</creatorcontrib><creatorcontrib>Bueno-Levy, Hanna</creatorcontrib><creatorcontrib>Umansky, Kfir Baruch</creatorcontrib><creatorcontrib>Mishaly, David</creatorcontrib><creatorcontrib>Shakked, Avraham</creatorcontrib><creatorcontrib>Miyara, Shoval</creatorcontrib><creatorcontrib>Sarusi-Portuguez, Avital</creatorcontrib><creatorcontrib>Goldfinger, Naomi</creatorcontrib><creatorcontrib>Prior, Amir</creatorcontrib><creatorcontrib>Morgenstern, David</creatorcontrib><creatorcontrib>Levin, Yishai</creatorcontrib><creatorcontrib>Addadi, Yoseph</creatorcontrib><creatorcontrib>Li, Baoguo</creatorcontrib><creatorcontrib>Rotter, Varda</creatorcontrib><creatorcontrib>Katz, Uriel</creatorcontrib><creatorcontrib>Tanaka, Elly M</creatorcontrib><creatorcontrib>Krizhanovsky, Valery</creatorcontrib><creatorcontrib>Sarig, Rachel</creatorcontrib><creatorcontrib>Tzahor, Eldad</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Nature Cardiovascular Research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhang, Lingling</au><au>Elkahal, Jacob</au><au>Wang, Tianzhen</au><au>Rimmer, Racheli</au><au>Genzelinakh, Alexander</au><au>Bassat, Elad</au><au>Wang, Jingkui</au><au>Perez, Dahlia</au><au>Kain, David</au><au>Lendengolts, Daria</au><au>Winkler, Roni</au><au>Bueno-Levy, Hanna</au><au>Umansky, Kfir Baruch</au><au>Mishaly, David</au><au>Shakked, Avraham</au><au>Miyara, Shoval</au><au>Sarusi-Portuguez, Avital</au><au>Goldfinger, Naomi</au><au>Prior, Amir</au><au>Morgenstern, David</au><au>Levin, Yishai</au><au>Addadi, Yoseph</au><au>Li, Baoguo</au><au>Rotter, Varda</au><au>Katz, Uriel</au><au>Tanaka, Elly M</au><au>Krizhanovsky, Valery</au><au>Sarig, Rachel</au><au>Tzahor, Eldad</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Egr1 regulates regenerative senescence and cardiac repair</atitle><jtitle>Nature Cardiovascular Research</jtitle><addtitle>Nat Cardiovasc Res</addtitle><date>2024-08-01</date><risdate>2024</risdate><volume>3</volume><issue>8</issue><spage>915</spage><epage>932</epage><pages>915-932</pages><issn>2731-0590</issn><eissn>2731-0590</eissn><abstract>Senescence plays a key role in various physiological and pathological processes. We reported that injury-induced transient senescence correlates with heart regeneration, yet the multi-omics profile and molecular underpinnings of regenerative senescence remain obscure. Using proteomics and single-cell RNA sequencing, here we report the regenerative senescence multi-omic signature in the adult mouse heart and establish its role in neonatal heart regeneration and agrin-mediated cardiac repair in adult mice. We identified early growth response protein 1 (Egr1) as a regulator of regenerative senescence in both models. In the neonatal heart, Egr1 facilitates angiogenesis and cardiomyocyte proliferation. In adult hearts, agrin-induced senescence and repair require Egr1, activated by the integrin-FAK-ERK-Akt1 axis in cardiac fibroblasts. We also identified cathepsins as injury-induced senescence-associated secretory phenotype components that promote extracellular matrix degradation and potentially assist in reducing fibrosis. Altogether, we uncovered the molecular signature and functional benefits of regenerative senescence during heart regeneration, with Egr1 orchestrating the process.</abstract><cop>England</cop><pmid>39196027</pmid><doi>10.1038/s44161-024-00493-1</doi><tpages>18</tpages><orcidid>https://orcid.org/0000-0002-0628-1443</orcidid><orcidid>https://orcid.org/0000-0003-0157-7162</orcidid><orcidid>https://orcid.org/0000-0002-9003-046X</orcidid><orcidid>https://orcid.org/0000-0002-5212-9426</orcidid><orcidid>https://orcid.org/0000-0001-9827-0436</orcidid><orcidid>https://orcid.org/0000-0003-4240-2158</orcidid><orcidid>https://orcid.org/0000-0003-0541-3069</orcidid><orcidid>https://orcid.org/0000-0002-4132-5114</orcidid></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 2731-0590 |
| ispartof | Nature Cardiovascular Research, 2024-08, Vol.3 (8), p.915-932 |
| issn | 2731-0590 2731-0590 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_3097855533 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Animals, Newborn Cell Proliferation Cells, Cultured Cellular Senescence - physiology Disease Models, Animal Early Growth Response Protein 1 - genetics Early Growth Response Protein 1 - metabolism Extracellular Signal-Regulated MAP Kinases - metabolism Fibroblasts - metabolism Focal Adhesion Kinase 1 Male Mice Mice, Inbred C57BL Mice, Knockout Myocytes, Cardiac - metabolism Neovascularization, Physiologic - physiology Proteomics Proto-Oncogene Proteins c-akt - metabolism Regeneration - physiology Senescence-Associated Secretory Phenotype Signal Transduction Single-Cell Analysis |
| title | Egr1 regulates regenerative senescence and cardiac repair |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-14T20%3A52%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=Egr1%20regulates%20regenerative%20senescence%20and%20cardiac%20repair&rft.jtitle=Nature%20Cardiovascular%20Research&rft.au=Zhang,%20Lingling&rft.date=2024-08-01&rft.volume=3&rft.issue=8&rft.spage=915&rft.epage=932&rft.pages=915-932&rft.issn=2731-0590&rft.eissn=2731-0590&rft_id=info:doi/10.1038/s44161-024-00493-1&rft_dat=%3Cproquest_cross%3E3097855533%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=3097855533&rft_id=info:pmid/39196027&rfr_iscdi=true |