Cathepsin B aggravates atherosclerosis in ApoE-deficient mice by modulating vascular smooth muscle cell pyroptosis through NF-κB / NLRP3 signaling pathway
Atherosclerosis (AS) is a chronic inflammatory disease involving cell death and inflammatory responses. Pyroptosis, a newly discovered pro-inflammatory programmed cell death process, exacerbates inflammatory responses. However, the roles of cathepsin B (CTSB) in pyroptosis and AS remain unclear. To...
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description | Atherosclerosis (AS) is a chronic inflammatory disease involving cell death and inflammatory responses. Pyroptosis, a newly discovered pro-inflammatory programmed cell death process, exacerbates inflammatory responses. However, the roles of cathepsin B (CTSB) in pyroptosis and AS remain unclear. To gain further insight, we fed ApoE-/- mice a high-fat diet to investigate the effects and mechanisms of CTSB overexpression and silencing on AS. We also explored the specific role of CTSB in vascular smooth muscle cells (VSMCs) in vitro. The study revealed that high-fat diet led to the formation of AS plaques, and CTSB was found to increase the AS plaque lesion area. Immunohistochemical and TUNEL/caspase-1 staining revealed the existence of pyroptosis in atherosclerotic plaques, particularly in VSMCs. In vitro studies, including Hoechst 33342/propidium iodide staining, a lactate dehydrogenase (LDH) release assay, detection of protein indicators of pyroptosis, and detection of interleukin-1β (IL-1β) in cell culture medium, demonstrated that oxidized low-density lipoprotein (ox-LDL) induced VSMC pyroptosis. Additionally, CTSB promoted VSMC pyroptosis. Ox-LDL increased the expression of CTSB, which in turn activated the NOD-like receptor protein 3 (NLRP3) inflammasome and promoted NLRP3 expression by facilitating nuclear factor kappa B (NF-κB) p65 nuclear translocation. This effect could be attenuated by the NF-κB inhibitor SN50. Our research found that CTSB not only promotes VSMC pyroptosis by activating the NLRP3 inflammasome, but also increases the expression of NLRP3. |
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Pyroptosis, a newly discovered pro-inflammatory programmed cell death process, exacerbates inflammatory responses. However, the roles of cathepsin B (CTSB) in pyroptosis and AS remain unclear. To gain further insight, we fed ApoE-/- mice a high-fat diet to investigate the effects and mechanisms of CTSB overexpression and silencing on AS. We also explored the specific role of CTSB in vascular smooth muscle cells (VSMCs) in vitro. The study revealed that high-fat diet led to the formation of AS plaques, and CTSB was found to increase the AS plaque lesion area. Immunohistochemical and TUNEL/caspase-1 staining revealed the existence of pyroptosis in atherosclerotic plaques, particularly in VSMCs. In vitro studies, including Hoechst 33342/propidium iodide staining, a lactate dehydrogenase (LDH) release assay, detection of protein indicators of pyroptosis, and detection of interleukin-1β (IL-1β) in cell culture medium, demonstrated that oxidized low-density lipoprotein (ox-LDL) induced VSMC pyroptosis. Additionally, CTSB promoted VSMC pyroptosis. Ox-LDL increased the expression of CTSB, which in turn activated the NOD-like receptor protein 3 (NLRP3) inflammasome and promoted NLRP3 expression by facilitating nuclear factor kappa B (NF-κB) p65 nuclear translocation. This effect could be attenuated by the NF-κB inhibitor SN50. Our research found that CTSB not only promotes VSMC pyroptosis by activating the NLRP3 inflammasome, but also increases the expression of NLRP3.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0294514</identifier><identifier>PMID: 38165884</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Antibodies ; Apolipoprotein E ; Apolipoproteins E - genetics ; Apoptosis ; Arteriosclerosis ; Atherosclerosis ; Atherosclerosis - metabolism ; Biology and Life Sciences ; Biotechnology industry ; Cardiovascular disease ; Caspase-1 ; Cathepsin B ; Cathepsin B - metabolism ; Cell culture ; Cell death ; Coronary vessels ; Dehydrogenases ; Diet ; Heart ; High fat diet ; Inflammasomes ; Inflammasomes - metabolism ; Inflammatory diseases ; Iodides ; L-Lactate dehydrogenase ; Laboratory animals ; Lactate dehydrogenase ; Low density lipoprotein ; Medicine and Health Sciences ; Mice ; Mice, Knockout, ApoE ; Muscle, Smooth, Vascular - metabolism ; Muscles ; NF-kappa B - metabolism ; NF-κB protein ; NLR Family, Pyrin Domain-Containing 3 Protein - metabolism ; Nuclear transport ; Plaque, Atherosclerotic - pathology ; Plaques ; Propidium iodide ; Proteins ; Pyroptosis ; Research and analysis methods ; Signal Transduction ; Smooth muscle ; Staining ; Stains & staining ; Translocation ; Tumor necrosis factor-TNF</subject><ispartof>PloS one, 2024-01, Vol.19 (1), p.e0294514-e0294514</ispartof><rights>Copyright: © 2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.</rights><rights>2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2024 Li et al 2024 Li et al</rights><rights>2024 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c476t-da5eae4159bd90d87b617351bc38370df01346ad3d48e3764646ec2644f7875f3</cites><orcidid>0009-0004-8852-1624</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10760722/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC10760722/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23865,27923,27924,53790,53792,79371,79372</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38165884$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Gou, Lingshan</contributor><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Zhao, Quanwei</creatorcontrib><creatorcontrib>Liu, Danan</creatorcontrib><creatorcontrib>Zhou, Bo</creatorcontrib><creatorcontrib>Liao, Fujun</creatorcontrib><creatorcontrib>Chen, Long</creatorcontrib><title>Cathepsin B aggravates atherosclerosis in ApoE-deficient mice by modulating vascular smooth muscle cell pyroptosis through NF-κB / NLRP3 signaling pathway</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Atherosclerosis (AS) is a chronic inflammatory disease involving cell death and inflammatory responses. Pyroptosis, a newly discovered pro-inflammatory programmed cell death process, exacerbates inflammatory responses. However, the roles of cathepsin B (CTSB) in pyroptosis and AS remain unclear. To gain further insight, we fed ApoE-/- mice a high-fat diet to investigate the effects and mechanisms of CTSB overexpression and silencing on AS. We also explored the specific role of CTSB in vascular smooth muscle cells (VSMCs) in vitro. The study revealed that high-fat diet led to the formation of AS plaques, and CTSB was found to increase the AS plaque lesion area. Immunohistochemical and TUNEL/caspase-1 staining revealed the existence of pyroptosis in atherosclerotic plaques, particularly in VSMCs. In vitro studies, including Hoechst 33342/propidium iodide staining, a lactate dehydrogenase (LDH) release assay, detection of protein indicators of pyroptosis, and detection of interleukin-1β (IL-1β) in cell culture medium, demonstrated that oxidized low-density lipoprotein (ox-LDL) induced VSMC pyroptosis. Additionally, CTSB promoted VSMC pyroptosis. Ox-LDL increased the expression of CTSB, which in turn activated the NOD-like receptor protein 3 (NLRP3) inflammasome and promoted NLRP3 expression by facilitating nuclear factor kappa B (NF-κB) p65 nuclear translocation. This effect could be attenuated by the NF-κB inhibitor SN50. Our research found that CTSB not only promotes VSMC pyroptosis by activating the NLRP3 inflammasome, but also increases the expression of NLRP3.</description><subject>Animals</subject><subject>Antibodies</subject><subject>Apolipoprotein E</subject><subject>Apolipoproteins E - genetics</subject><subject>Apoptosis</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Atherosclerosis - metabolism</subject><subject>Biology and Life Sciences</subject><subject>Biotechnology industry</subject><subject>Cardiovascular disease</subject><subject>Caspase-1</subject><subject>Cathepsin B</subject><subject>Cathepsin B - metabolism</subject><subject>Cell culture</subject><subject>Cell death</subject><subject>Coronary vessels</subject><subject>Dehydrogenases</subject><subject>Diet</subject><subject>Heart</subject><subject>High fat diet</subject><subject>Inflammasomes</subject><subject>Inflammasomes - metabolism</subject><subject>Inflammatory diseases</subject><subject>Iodides</subject><subject>L-Lactate dehydrogenase</subject><subject>Laboratory animals</subject><subject>Lactate dehydrogenase</subject><subject>Low density lipoprotein</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Knockout, ApoE</subject><subject>Muscle, Smooth, Vascular - metabolism</subject><subject>Muscles</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</subject><subject>Nuclear transport</subject><subject>Plaque, Atherosclerotic - pathology</subject><subject>Plaques</subject><subject>Propidium iodide</subject><subject>Proteins</subject><subject>Pyroptosis</subject><subject>Research and analysis methods</subject><subject>Signal Transduction</subject><subject>Smooth muscle</subject><subject>Staining</subject><subject>Stains & staining</subject><subject>Translocation</subject><subject>Tumor necrosis factor-TNF</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</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><sourceid>DOA</sourceid><recordid>eNptUttu1DAQjRCIXuAPEFjihZdsfYvjPKF21UKlVUEIni3HdhKvkjjYyaL9Fv6kH8E34XTTqkXIkmc0c-aMz3iS5A2CK0RydLZ1k-9luxpcb1YQFzRD9FlyjAqCU4Yhef7IP0pOQthCmBHO2MvkiHDEMs7pcfJ7LcfGDMH24ALIuvZyJ0cTwBz1Lqh2vm0AMX8-uMtUm8oqa_oRdFYZUO5B5_TUytH2NdjJoKLvQeicGxvQTTMBUKZtwbD3bhjvuMbGu6luwM1V-uf2ApyBm823rwQEW0c9M88Qu_-S-1fJi0q2wbxe7Gny4-ry-_pzuvny6Xp9vkkVzdmYapkZaSjKilIXUPO8ZCgnGSoV4SSHuoKIUCY10ZQbkjMaj1GYUVrlPM8qcpq8O_AOrQtimWsQBLICQ4whjYjrA0I7uRWDt530e-GkFXcB52sh_WijWGEQhwVWOpNYUxkNwspopGimGGcER66PS7ep7IxWcZZetk9In2Z624ja7QSCOYM5nhk-LAze_ZxMGEVnwzxk2Rs3BYELWDBYUMoi9P0_0P_LoweUip8dvKkeXoOgmJftvkrMyyaWZYtlbx8reSi63y7yFzqA1X4</recordid><startdate>20240101</startdate><enddate>20240101</enddate><creator>Li, Hui</creator><creator>Zhao, Quanwei</creator><creator>Liu, Danan</creator><creator>Zhou, Bo</creator><creator>Liao, Fujun</creator><creator>Chen, Long</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0009-0004-8852-1624</orcidid></search><sort><creationdate>20240101</creationdate><title>Cathepsin B aggravates atherosclerosis in ApoE-deficient mice by modulating vascular smooth muscle cell pyroptosis through NF-κB / NLRP3 signaling pathway</title><author>Li, Hui ; Zhao, Quanwei ; Liu, Danan ; Zhou, Bo ; Liao, Fujun ; Chen, Long</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c476t-da5eae4159bd90d87b617351bc38370df01346ad3d48e3764646ec2644f7875f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Antibodies</topic><topic>Apolipoprotein E</topic><topic>Apolipoproteins E - genetics</topic><topic>Apoptosis</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Atherosclerosis - metabolism</topic><topic>Biology and Life Sciences</topic><topic>Biotechnology industry</topic><topic>Cardiovascular disease</topic><topic>Caspase-1</topic><topic>Cathepsin B</topic><topic>Cathepsin B - metabolism</topic><topic>Cell culture</topic><topic>Cell death</topic><topic>Coronary vessels</topic><topic>Dehydrogenases</topic><topic>Diet</topic><topic>Heart</topic><topic>High fat diet</topic><topic>Inflammasomes</topic><topic>Inflammasomes - metabolism</topic><topic>Inflammatory diseases</topic><topic>Iodides</topic><topic>L-Lactate dehydrogenase</topic><topic>Laboratory animals</topic><topic>Lactate dehydrogenase</topic><topic>Low density lipoprotein</topic><topic>Medicine and Health Sciences</topic><topic>Mice</topic><topic>Mice, Knockout, ApoE</topic><topic>Muscle, Smooth, Vascular - metabolism</topic><topic>Muscles</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB protein</topic><topic>NLR Family, Pyrin Domain-Containing 3 Protein - metabolism</topic><topic>Nuclear transport</topic><topic>Plaque, Atherosclerotic - pathology</topic><topic>Plaques</topic><topic>Propidium iodide</topic><topic>Proteins</topic><topic>Pyroptosis</topic><topic>Research and analysis methods</topic><topic>Signal Transduction</topic><topic>Smooth muscle</topic><topic>Staining</topic><topic>Stains & staining</topic><topic>Translocation</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Hui</creatorcontrib><creatorcontrib>Zhao, Quanwei</creatorcontrib><creatorcontrib>Liu, Danan</creatorcontrib><creatorcontrib>Zhou, Bo</creatorcontrib><creatorcontrib>Liao, Fujun</creatorcontrib><creatorcontrib>Chen, Long</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>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Proquest Nursing & Allied Health Source</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</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 & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Hui</au><au>Zhao, Quanwei</au><au>Liu, Danan</au><au>Zhou, Bo</au><au>Liao, Fujun</au><au>Chen, Long</au><au>Gou, Lingshan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cathepsin B aggravates atherosclerosis in ApoE-deficient mice by modulating vascular smooth muscle cell pyroptosis through NF-κB / NLRP3 signaling pathway</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2024-01-01</date><risdate>2024</risdate><volume>19</volume><issue>1</issue><spage>e0294514</spage><epage>e0294514</epage><pages>e0294514-e0294514</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Atherosclerosis (AS) is a chronic inflammatory disease involving cell death and inflammatory responses. Pyroptosis, a newly discovered pro-inflammatory programmed cell death process, exacerbates inflammatory responses. However, the roles of cathepsin B (CTSB) in pyroptosis and AS remain unclear. To gain further insight, we fed ApoE-/- mice a high-fat diet to investigate the effects and mechanisms of CTSB overexpression and silencing on AS. We also explored the specific role of CTSB in vascular smooth muscle cells (VSMCs) in vitro. The study revealed that high-fat diet led to the formation of AS plaques, and CTSB was found to increase the AS plaque lesion area. Immunohistochemical and TUNEL/caspase-1 staining revealed the existence of pyroptosis in atherosclerotic plaques, particularly in VSMCs. In vitro studies, including Hoechst 33342/propidium iodide staining, a lactate dehydrogenase (LDH) release assay, detection of protein indicators of pyroptosis, and detection of interleukin-1β (IL-1β) in cell culture medium, demonstrated that oxidized low-density lipoprotein (ox-LDL) induced VSMC pyroptosis. Additionally, CTSB promoted VSMC pyroptosis. Ox-LDL increased the expression of CTSB, which in turn activated the NOD-like receptor protein 3 (NLRP3) inflammasome and promoted NLRP3 expression by facilitating nuclear factor kappa B (NF-κB) p65 nuclear translocation. This effect could be attenuated by the NF-κB inhibitor SN50. Our research found that CTSB not only promotes VSMC pyroptosis by activating the NLRP3 inflammasome, but also increases the expression of NLRP3.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>38165884</pmid><doi>10.1371/journal.pone.0294514</doi><orcidid>https://orcid.org/0009-0004-8852-1624</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Antibodies Apolipoprotein E Apolipoproteins E - genetics Apoptosis Arteriosclerosis Atherosclerosis Atherosclerosis - metabolism Biology and Life Sciences Biotechnology industry Cardiovascular disease Caspase-1 Cathepsin B Cathepsin B - metabolism Cell culture Cell death Coronary vessels Dehydrogenases Diet Heart High fat diet Inflammasomes Inflammasomes - metabolism Inflammatory diseases Iodides L-Lactate dehydrogenase Laboratory animals Lactate dehydrogenase Low density lipoprotein Medicine and Health Sciences Mice Mice, Knockout, ApoE Muscle, Smooth, Vascular - metabolism Muscles NF-kappa B - metabolism NF-κB protein NLR Family, Pyrin Domain-Containing 3 Protein - metabolism Nuclear transport Plaque, Atherosclerotic - pathology Plaques Propidium iodide Proteins Pyroptosis Research and analysis methods Signal Transduction Smooth muscle Staining Stains & staining Translocation Tumor necrosis factor-TNF |
title | Cathepsin B aggravates atherosclerosis in ApoE-deficient mice by modulating vascular smooth muscle cell pyroptosis through NF-κB / NLRP3 signaling pathway |
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