Loading…
Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy
Age and age-dependent inflammation are two main risk factors for cardiovascular diseases. Aging can also affect clock gene-related impairments such as chronodisruption and has been linked to a decline in melatonin synthesis and aggravation of the NF-κB/NLRP3 innate immune response known as inflammag...
Saved in:
Published in: | International journal of molecular sciences 2022-06, Vol.23 (12), p.6846 |
---|---|
Main Authors: | , , , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
cited_by | cdi_FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613 |
---|---|
cites | cdi_FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613 |
container_end_page | |
container_issue | 12 |
container_start_page | 6846 |
container_title | International journal of molecular sciences |
container_volume | 23 |
creator | Fernández-Ortiz, Marisol Sayed, Ramy K. A. Román-Montoya, Yolanda de Lama, María Ángeles Rol Fernández-Martínez, José Ramírez-Casas, Yolanda Florido-Ruiz, Javier Rusanova, Iryna Escames, Germaine Acuña-Castroviejo, Darío |
description | Age and age-dependent inflammation are two main risk factors for cardiovascular diseases. Aging can also affect clock gene-related impairments such as chronodisruption and has been linked to a decline in melatonin synthesis and aggravation of the NF-κB/NLRP3 innate immune response known as inflammaging. The molecular drivers of these mechanisms remain unknown. This study investigated the impact of aging and NLRP3 expression on the cardiac circadian system, and the actions of melatonin as a potential therapy to restore daily rhythms by mitigating inflammaging. We analyzed the circadian expression and rhythmicity of clock genes in heart tissue of wild-type and NLRP3-knockout mice at 3, 12, and 24 months of age, with and without melatonin treatment. Our results support that aging, NLRP3 inflammasome, and melatonin affected the cardiac clock genes expression, except for Rev-erbα, which was not influenced by genotype. Aging caused small phase changes in Clock, loss of rhythmicity in Per2 and Rorα, and mesor dampening of Clock, Bmal1, and Per2. NLRP3 inflammasome influenced the acrophase of Clock, Per2, and Rorα. Melatonin restored the acrophase and the rhythm of clock genes affected by age or NLRP3 activation. The administration of melatonin re-established murine cardiac homeostasis by reversing age-associated chronodisruption. Altogether, these results highlight new findings about the effects aging and NLRP3 inflammasome have on clock genes in cardiac tissue, pointing to continuous melatonin as a promising therapy to placate inflammaging and restore circadian rhythm in heart muscle. Additionally, light microscopy analysis showed age-related morphological impairments in cardiomyocytes, which were less severe in mice lacking NLRP3. Melatonin supplementation preserved the structure of cardiac muscle fibers in all experimental groups. |
doi_str_mv | 10.3390/ijms23126846 |
format | article |
fullrecord | <record><control><sourceid>proquest_doaj_</sourceid><recordid>TN_cdi_doaj_primary_oai_doaj_org_article_b4eaea58b2fe4d6fa1e16bdea700eb65</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_b4eaea58b2fe4d6fa1e16bdea700eb65</doaj_id><sourcerecordid>2679753456</sourcerecordid><originalsourceid>FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613</originalsourceid><addsrcrecordid>eNpdkk1vEzEQhlcIRD_gxg-wxIUDAX9_cECqotJGSgGhcrZs7zjZaNcO9gap_x6XVKjl4rE87zwavzNd94bgD4wZ_HHYTZUyQqXm8ll3SjilC4ylev7oftKd1brDmDIqzMvuhAnFGdX6tLMXG0Au9Wi5LTnlfqjlsJ-HnNCQ0E0-VEDX4Mr8CV3GCGFGOaJ5C-jr-sd3hlYpjm6aXM3TkXIDo5tzarW3Wyhuf_eqexHdWOH1Qzzvfn65vF1eL9bfrlbLi_UicCHmhRJcSyMV0dJzAtgYFUz0EnsTgxY0EOgjI8EoCkL2zDPpNcVeEuF1O9l5tzpy--x2dl-GyZU7m91g_z7ksrHtF0MYwXoODpzQnkbgvYyOAJG-B6cwBi9FY30-svYHP0EfIM3FjU-gTzNp2NpN_m0NpZwp2QDvHgAl_zpAne001ADj6BI0S22bFcGcYs2b9O1_0l0-lNSsaipllGBc3APfH1Wh5FoLxH_NEGzvt8A-3gL2B8Bao5E</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2679753456</pqid></control><display><type>article</type><title>Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy</title><source>Open Access: PubMed Central</source><source>Publicly Available Content Database</source><creator>Fernández-Ortiz, Marisol ; Sayed, Ramy K. A. ; Román-Montoya, Yolanda ; de Lama, María Ángeles Rol ; Fernández-Martínez, José ; Ramírez-Casas, Yolanda ; Florido-Ruiz, Javier ; Rusanova, Iryna ; Escames, Germaine ; Acuña-Castroviejo, Darío</creator><creatorcontrib>Fernández-Ortiz, Marisol ; Sayed, Ramy K. A. ; Román-Montoya, Yolanda ; de Lama, María Ángeles Rol ; Fernández-Martínez, José ; Ramírez-Casas, Yolanda ; Florido-Ruiz, Javier ; Rusanova, Iryna ; Escames, Germaine ; Acuña-Castroviejo, Darío</creatorcontrib><description>Age and age-dependent inflammation are two main risk factors for cardiovascular diseases. Aging can also affect clock gene-related impairments such as chronodisruption and has been linked to a decline in melatonin synthesis and aggravation of the NF-κB/NLRP3 innate immune response known as inflammaging. The molecular drivers of these mechanisms remain unknown. This study investigated the impact of aging and NLRP3 expression on the cardiac circadian system, and the actions of melatonin as a potential therapy to restore daily rhythms by mitigating inflammaging. We analyzed the circadian expression and rhythmicity of clock genes in heart tissue of wild-type and NLRP3-knockout mice at 3, 12, and 24 months of age, with and without melatonin treatment. Our results support that aging, NLRP3 inflammasome, and melatonin affected the cardiac clock genes expression, except for Rev-erbα, which was not influenced by genotype. Aging caused small phase changes in Clock, loss of rhythmicity in Per2 and Rorα, and mesor dampening of Clock, Bmal1, and Per2. NLRP3 inflammasome influenced the acrophase of Clock, Per2, and Rorα. Melatonin restored the acrophase and the rhythm of clock genes affected by age or NLRP3 activation. The administration of melatonin re-established murine cardiac homeostasis by reversing age-associated chronodisruption. Altogether, these results highlight new findings about the effects aging and NLRP3 inflammasome have on clock genes in cardiac tissue, pointing to continuous melatonin as a promising therapy to placate inflammaging and restore circadian rhythm in heart muscle. Additionally, light microscopy analysis showed age-related morphological impairments in cardiomyocytes, which were less severe in mice lacking NLRP3. Melatonin supplementation preserved the structure of cardiac muscle fibers in all experimental groups.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms23126846</identifier><identifier>PMID: 35743288</identifier><language>eng</language><publisher>Basel: MDPI AG</publisher><subject>Age ; Aging ; BMAL1 protein ; Cardiac muscle ; Cardiomyocytes ; Cardiovascular diseases ; Chronic illnesses ; chronodisruption ; Circadian rhythm ; Circadian rhythms ; Clock gene ; clock genes ; Gene expression ; Genes ; Genotype & phenotype ; Genotypes ; Heart ; Homeostasis ; Immune response ; inflammaging ; Inflammasomes ; Innate immunity ; Light microscopy ; Melatonin ; Mitochondria ; Muscles ; NF-κB protein ; Optical microscopy ; Period 2 protein ; Physiology ; rhythm ; Risk analysis ; Risk factors ; Rodents</subject><ispartof>International journal of molecular sciences, 2022-06, Vol.23 (12), p.6846</ispartof><rights>2022 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2022 by the authors. 2022</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613</citedby><cites>FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613</cites><orcidid>0000-0002-9034-7600 ; 0000-0002-5334-9009 ; 0000-0002-5593-6733 ; 0000-0003-0556-852X ; 0000-0002-9680-1560 ; 0000-0003-4467-6742 ; 0000-0001-7541-4898 ; 0000-0003-1256-7656</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2679753456/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2679753456?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids></links><search><creatorcontrib>Fernández-Ortiz, Marisol</creatorcontrib><creatorcontrib>Sayed, Ramy K. A.</creatorcontrib><creatorcontrib>Román-Montoya, Yolanda</creatorcontrib><creatorcontrib>de Lama, María Ángeles Rol</creatorcontrib><creatorcontrib>Fernández-Martínez, José</creatorcontrib><creatorcontrib>Ramírez-Casas, Yolanda</creatorcontrib><creatorcontrib>Florido-Ruiz, Javier</creatorcontrib><creatorcontrib>Rusanova, Iryna</creatorcontrib><creatorcontrib>Escames, Germaine</creatorcontrib><creatorcontrib>Acuña-Castroviejo, Darío</creatorcontrib><title>Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy</title><title>International journal of molecular sciences</title><description>Age and age-dependent inflammation are two main risk factors for cardiovascular diseases. Aging can also affect clock gene-related impairments such as chronodisruption and has been linked to a decline in melatonin synthesis and aggravation of the NF-κB/NLRP3 innate immune response known as inflammaging. The molecular drivers of these mechanisms remain unknown. This study investigated the impact of aging and NLRP3 expression on the cardiac circadian system, and the actions of melatonin as a potential therapy to restore daily rhythms by mitigating inflammaging. We analyzed the circadian expression and rhythmicity of clock genes in heart tissue of wild-type and NLRP3-knockout mice at 3, 12, and 24 months of age, with and without melatonin treatment. Our results support that aging, NLRP3 inflammasome, and melatonin affected the cardiac clock genes expression, except for Rev-erbα, which was not influenced by genotype. Aging caused small phase changes in Clock, loss of rhythmicity in Per2 and Rorα, and mesor dampening of Clock, Bmal1, and Per2. NLRP3 inflammasome influenced the acrophase of Clock, Per2, and Rorα. Melatonin restored the acrophase and the rhythm of clock genes affected by age or NLRP3 activation. The administration of melatonin re-established murine cardiac homeostasis by reversing age-associated chronodisruption. Altogether, these results highlight new findings about the effects aging and NLRP3 inflammasome have on clock genes in cardiac tissue, pointing to continuous melatonin as a promising therapy to placate inflammaging and restore circadian rhythm in heart muscle. Additionally, light microscopy analysis showed age-related morphological impairments in cardiomyocytes, which were less severe in mice lacking NLRP3. Melatonin supplementation preserved the structure of cardiac muscle fibers in all experimental groups.</description><subject>Age</subject><subject>Aging</subject><subject>BMAL1 protein</subject><subject>Cardiac muscle</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular diseases</subject><subject>Chronic illnesses</subject><subject>chronodisruption</subject><subject>Circadian rhythm</subject><subject>Circadian rhythms</subject><subject>Clock gene</subject><subject>clock genes</subject><subject>Gene expression</subject><subject>Genes</subject><subject>Genotype & phenotype</subject><subject>Genotypes</subject><subject>Heart</subject><subject>Homeostasis</subject><subject>Immune response</subject><subject>inflammaging</subject><subject>Inflammasomes</subject><subject>Innate immunity</subject><subject>Light microscopy</subject><subject>Melatonin</subject><subject>Mitochondria</subject><subject>Muscles</subject><subject>NF-κB protein</subject><subject>Optical microscopy</subject><subject>Period 2 protein</subject><subject>Physiology</subject><subject>rhythm</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Rodents</subject><issn>1422-0067</issn><issn>1661-6596</issn><issn>1422-0067</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>DOA</sourceid><recordid>eNpdkk1vEzEQhlcIRD_gxg-wxIUDAX9_cECqotJGSgGhcrZs7zjZaNcO9gap_x6XVKjl4rE87zwavzNd94bgD4wZ_HHYTZUyQqXm8ll3SjilC4ylev7oftKd1brDmDIqzMvuhAnFGdX6tLMXG0Au9Wi5LTnlfqjlsJ-HnNCQ0E0-VEDX4Mr8CV3GCGFGOaJ5C-jr-sd3hlYpjm6aXM3TkXIDo5tzarW3Wyhuf_eqexHdWOH1Qzzvfn65vF1eL9bfrlbLi_UicCHmhRJcSyMV0dJzAtgYFUz0EnsTgxY0EOgjI8EoCkL2zDPpNcVeEuF1O9l5tzpy--x2dl-GyZU7m91g_z7ksrHtF0MYwXoODpzQnkbgvYyOAJG-B6cwBi9FY30-svYHP0EfIM3FjU-gTzNp2NpN_m0NpZwp2QDvHgAl_zpAne001ADj6BI0S22bFcGcYs2b9O1_0l0-lNSsaipllGBc3APfH1Wh5FoLxH_NEGzvt8A-3gL2B8Bao5E</recordid><startdate>20220620</startdate><enddate>20220620</enddate><creator>Fernández-Ortiz, Marisol</creator><creator>Sayed, Ramy K. A.</creator><creator>Román-Montoya, Yolanda</creator><creator>de Lama, María Ángeles Rol</creator><creator>Fernández-Martínez, José</creator><creator>Ramírez-Casas, Yolanda</creator><creator>Florido-Ruiz, Javier</creator><creator>Rusanova, Iryna</creator><creator>Escames, Germaine</creator><creator>Acuña-Castroviejo, Darío</creator><general>MDPI AG</general><general>MDPI</general><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-9034-7600</orcidid><orcidid>https://orcid.org/0000-0002-5334-9009</orcidid><orcidid>https://orcid.org/0000-0002-5593-6733</orcidid><orcidid>https://orcid.org/0000-0003-0556-852X</orcidid><orcidid>https://orcid.org/0000-0002-9680-1560</orcidid><orcidid>https://orcid.org/0000-0003-4467-6742</orcidid><orcidid>https://orcid.org/0000-0001-7541-4898</orcidid><orcidid>https://orcid.org/0000-0003-1256-7656</orcidid></search><sort><creationdate>20220620</creationdate><title>Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy</title><author>Fernández-Ortiz, Marisol ; Sayed, Ramy K. A. ; Román-Montoya, Yolanda ; de Lama, María Ángeles Rol ; Fernández-Martínez, José ; Ramírez-Casas, Yolanda ; Florido-Ruiz, Javier ; Rusanova, Iryna ; Escames, Germaine ; Acuña-Castroviejo, Darío</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>Age</topic><topic>Aging</topic><topic>BMAL1 protein</topic><topic>Cardiac muscle</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular diseases</topic><topic>Chronic illnesses</topic><topic>chronodisruption</topic><topic>Circadian rhythm</topic><topic>Circadian rhythms</topic><topic>Clock gene</topic><topic>clock genes</topic><topic>Gene expression</topic><topic>Genes</topic><topic>Genotype & phenotype</topic><topic>Genotypes</topic><topic>Heart</topic><topic>Homeostasis</topic><topic>Immune response</topic><topic>inflammaging</topic><topic>Inflammasomes</topic><topic>Innate immunity</topic><topic>Light microscopy</topic><topic>Melatonin</topic><topic>Mitochondria</topic><topic>Muscles</topic><topic>NF-κB protein</topic><topic>Optical microscopy</topic><topic>Period 2 protein</topic><topic>Physiology</topic><topic>rhythm</topic><topic>Risk analysis</topic><topic>Risk factors</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fernández-Ortiz, Marisol</creatorcontrib><creatorcontrib>Sayed, Ramy K. A.</creatorcontrib><creatorcontrib>Román-Montoya, Yolanda</creatorcontrib><creatorcontrib>de Lama, María Ángeles Rol</creatorcontrib><creatorcontrib>Fernández-Martínez, José</creatorcontrib><creatorcontrib>Ramírez-Casas, Yolanda</creatorcontrib><creatorcontrib>Florido-Ruiz, Javier</creatorcontrib><creatorcontrib>Rusanova, Iryna</creatorcontrib><creatorcontrib>Escames, Germaine</creatorcontrib><creatorcontrib>Acuña-Castroviejo, Darío</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health and Medical</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>ProQuest Central</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>ProQuest Research Library</collection><collection>Research Library (Corporate)</collection><collection>Publicly Available Content 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 China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>International journal of molecular sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fernández-Ortiz, Marisol</au><au>Sayed, Ramy K. A.</au><au>Román-Montoya, Yolanda</au><au>de Lama, María Ángeles Rol</au><au>Fernández-Martínez, José</au><au>Ramírez-Casas, Yolanda</au><au>Florido-Ruiz, Javier</au><au>Rusanova, Iryna</au><au>Escames, Germaine</au><au>Acuña-Castroviejo, Darío</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy</atitle><jtitle>International journal of molecular sciences</jtitle><date>2022-06-20</date><risdate>2022</risdate><volume>23</volume><issue>12</issue><spage>6846</spage><pages>6846-</pages><issn>1422-0067</issn><issn>1661-6596</issn><eissn>1422-0067</eissn><abstract>Age and age-dependent inflammation are two main risk factors for cardiovascular diseases. Aging can also affect clock gene-related impairments such as chronodisruption and has been linked to a decline in melatonin synthesis and aggravation of the NF-κB/NLRP3 innate immune response known as inflammaging. The molecular drivers of these mechanisms remain unknown. This study investigated the impact of aging and NLRP3 expression on the cardiac circadian system, and the actions of melatonin as a potential therapy to restore daily rhythms by mitigating inflammaging. We analyzed the circadian expression and rhythmicity of clock genes in heart tissue of wild-type and NLRP3-knockout mice at 3, 12, and 24 months of age, with and without melatonin treatment. Our results support that aging, NLRP3 inflammasome, and melatonin affected the cardiac clock genes expression, except for Rev-erbα, which was not influenced by genotype. Aging caused small phase changes in Clock, loss of rhythmicity in Per2 and Rorα, and mesor dampening of Clock, Bmal1, and Per2. NLRP3 inflammasome influenced the acrophase of Clock, Per2, and Rorα. Melatonin restored the acrophase and the rhythm of clock genes affected by age or NLRP3 activation. The administration of melatonin re-established murine cardiac homeostasis by reversing age-associated chronodisruption. Altogether, these results highlight new findings about the effects aging and NLRP3 inflammasome have on clock genes in cardiac tissue, pointing to continuous melatonin as a promising therapy to placate inflammaging and restore circadian rhythm in heart muscle. Additionally, light microscopy analysis showed age-related morphological impairments in cardiomyocytes, which were less severe in mice lacking NLRP3. Melatonin supplementation preserved the structure of cardiac muscle fibers in all experimental groups.</abstract><cop>Basel</cop><pub>MDPI AG</pub><pmid>35743288</pmid><doi>10.3390/ijms23126846</doi><orcidid>https://orcid.org/0000-0002-9034-7600</orcidid><orcidid>https://orcid.org/0000-0002-5334-9009</orcidid><orcidid>https://orcid.org/0000-0002-5593-6733</orcidid><orcidid>https://orcid.org/0000-0003-0556-852X</orcidid><orcidid>https://orcid.org/0000-0002-9680-1560</orcidid><orcidid>https://orcid.org/0000-0003-4467-6742</orcidid><orcidid>https://orcid.org/0000-0001-7541-4898</orcidid><orcidid>https://orcid.org/0000-0003-1256-7656</orcidid><oa>free_for_read</oa></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1422-0067 |
ispartof | International journal of molecular sciences, 2022-06, Vol.23 (12), p.6846 |
issn | 1422-0067 1661-6596 1422-0067 |
language | eng |
recordid | cdi_doaj_primary_oai_doaj_org_article_b4eaea58b2fe4d6fa1e16bdea700eb65 |
source | Open Access: PubMed Central; Publicly Available Content Database |
subjects | Age Aging BMAL1 protein Cardiac muscle Cardiomyocytes Cardiovascular diseases Chronic illnesses chronodisruption Circadian rhythm Circadian rhythms Clock gene clock genes Gene expression Genes Genotype & phenotype Genotypes Heart Homeostasis Immune response inflammaging Inflammasomes Innate immunity Light microscopy Melatonin Mitochondria Muscles NF-κB protein Optical microscopy Period 2 protein Physiology rhythm Risk analysis Risk factors Rodents |
title | Age and Chronodisruption in Mouse Heart: Effect of the NLRP3 Inflammasome and Melatonin Therapy |
url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T13%3A44%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Age%20and%20Chronodisruption%20in%20Mouse%20Heart:%20Effect%20of%20the%20NLRP3%20Inflammasome%20and%20Melatonin%20Therapy&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Fern%C3%A1ndez-Ortiz,%20Marisol&rft.date=2022-06-20&rft.volume=23&rft.issue=12&rft.spage=6846&rft.pages=6846-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms23126846&rft_dat=%3Cproquest_doaj_%3E2679753456%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c455t-75486967186b41e0997c9fb60b9fc852c1edf31c972e56d3b36b820b615b8b613%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2679753456&rft_id=info:pmid/35743288&rfr_iscdi=true |