FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2897516832> ?p ?o ?g. }

• W2897516832 endingPage "1792" @default.
• W2897516832 startingPage "1782" @default.
• W2897516832 abstract "Previous evidence has indicated a beneficial role for aldehyde dehydrogenase 2 (ALDH2) in suppressing atherosclerotic plaque progression and instability. However, the underlying mechanism remains somewhat elusive. This study was designed to examine the effect of ALDH2 deficiency on high-cholesterol diet-induced atherosclerotic plaque progression and plaque vulnerability in atherosclerosis-prone ApoE knockout (ApoE−/−) mice with a focus on foam cell formation in macrophages and senescence of vascular smooth muscle cells (VSMCs). Serum lipid profile, plaque progression, and plaque vulnerability were examined in ApoE−/− and ALDH2/ApoE double knockout (ALDH2−/−ApoE−/−) mice after high-cholesterol diet intake for 8 weeks. ALDH2 deficiency increased the serum levels of triglycerides while it decreased levels of total cholesterol and high-density lipoprotein cholesterol. Unexpectedly, ALDH2 deficiency reduced the plaque area by 58.9% and 37.5% in aorta and aortic sinus, respectively. Plaque instability was aggravated by ALDH2 deficiency along with the increased necrotic core size, decreased collagen content, thinner fibrous cap area, decreased VSMC content, and increased macrophage content. In atherosclerotic lesions, ALDH2 protein was located in both macrophages and VSMCs. Further results revealed downregulated ALDH2 expression in aorta of aged ApoE−/− mice compared with young mice. However, in vitro study suggested that ALDH2 expression was upregulated in bone marrow-derived macrophages (BMDMs) with an opposite effect in VSMCs following 80 μg/ml oxidized low-density lipoprotein (oxLDL) treatment. Interestingly, ALDH2 deficiency displayed little effect in oxLDL-induced foam cell formation from BMDMs, while ALDH2 knockdown by siRNA and ALDH2 overexpression by lentivirus infection promoted and retarded oxLDL-induced VSMC senescence, respectively. Mechanistically, ALDH2 mitigated oxLDL-induced overproduction of mitochondrial reactive oxygen species (mROS) and activation of downstream p53/p21/p16 pathway. Clearance of mROS by mitoTEMPO significantly reversed the promotive effect of ALDH2 knockdown on VSMC senescence. Taken together, our data revealed that ALDH2 deficiency suppressed atherosclerotic plaque area while facilitating plaque instability possibly through accelerating mROS-mediated VSMC senescence. This article is part of a Special Issue entitled: Genetic and epigenetic regulation of aging and longevity edited by Jun Ren & Megan Yingmei Zhang." @default.
• W2897516832 created "2018-10-26" @default.
• W2897516832 creator A5002008253 @default.
• W2897516832 creator A5003096114 @default.
• W2897516832 creator A5004394267 @default.
• W2897516832 creator A5009579813 @default.
• W2897516832 creator A5019641117 @default.
• W2897516832 creator A5020763510 @default.
• W2897516832 creator A5024401560 @default.
• W2897516832 creator A5030825527 @default.
• W2897516832 creator A5046078938 @default.
• W2897516832 creator A5053512076 @default.
• W2897516832 creator A5053743858 @default.
• W2897516832 creator A5054933672 @default.
• W2897516832 creator A5065560361 @default.
• W2897516832 creator A5075539250 @default.
• W2897516832 creator A5078164215 @default.
• W2897516832 creator A5087437644 @default.
• W2897516832 date "2019-07-01" @default.
• W2897516832 modified "2023-10-02" @default.
• W2897516832 title "Aldehyde dehydrogenase 2 deficiency promotes atherosclerotic plaque instability through accelerating mitochondrial ROS-mediated vascular smooth muscle cell senescence" @default.
• W2897516832 cites W1535736016 @default.
• W2897516832 cites W1836984528 @default.
• W2897516832 cites W1979271332 @default.
• W2897516832 cites W1985939862 @default.
• W2897516832 cites W1988040246 @default.
• W2897516832 cites W1991767791 @default.
• W2897516832 cites W2005627263 @default.
• W2897516832 cites W2009334494 @default.
• W2897516832 cites W2028732326 @default.
• W2897516832 cites W2031743773 @default.
• W2897516832 cites W2034142770 @default.
• W2897516832 cites W2047208185 @default.
• W2897516832 cites W2070663300 @default.
• W2897516832 cites W2091034186 @default.
• W2897516832 cites W2106814762 @default.
• W2897516832 cites W2113934014 @default.
• W2897516832 cites W2118568491 @default.
• W2897516832 cites W2119210523 @default.
• W2897516832 cites W2124349235 @default.
• W2897516832 cites W2127634832 @default.
• W2897516832 cites W2143831767 @default.
• W2897516832 cites W2147181044 @default.
• W2897516832 cites W2150795824 @default.
• W2897516832 cites W2160156045 @default.
• W2897516832 cites W2169582356 @default.
• W2897516832 cites W2170684837 @default.
• W2897516832 cites W2172797119 @default.
• W2897516832 cites W2357868452 @default.
• W2897516832 cites W2409677060 @default.
• W2897516832 cites W2470621842 @default.
• W2897516832 cites W2484553766 @default.
• W2897516832 cites W2497971182 @default.
• W2897516832 cites W2521275176 @default.
• W2897516832 cites W2529676469 @default.
• W2897516832 cites W2530714323 @default.
• W2897516832 cites W2663531814 @default.
• W2897516832 cites W2751622885 @default.
• W2897516832 cites W2778404574 @default.
• W2897516832 cites W2792785502 @default.
• W2897516832 cites W2804648321 @default.
• W2897516832 cites W2806648923 @default.
• W2897516832 cites W2896260097 @default.
• W2897516832 doi "https://doi.org/10.1016/j.bbadis.2018.09.033" @default.
• W2897516832 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30315930" @default.
• W2897516832 hasPublicationYear "2019" @default.
• W2897516832 type Work @default.
• W2897516832 sameAs 2897516832 @default.
• W2897516832 citedByCount "23" @default.
• W2897516832 countsByYear W28975168322019 @default.
• W2897516832 countsByYear W28975168322020 @default.
• W2897516832 countsByYear W28975168322021 @default.
• W2897516832 countsByYear W28975168322022 @default.
• W2897516832 countsByYear W28975168322023 @default.
• W2897516832 crossrefType "journal-article" @default.
• W2897516832 hasAuthorship W2897516832A5002008253 @default.
• W2897516832 hasAuthorship W2897516832A5003096114 @default.
• W2897516832 hasAuthorship W2897516832A5004394267 @default.
• W2897516832 hasAuthorship W2897516832A5009579813 @default.
• W2897516832 hasAuthorship W2897516832A5019641117 @default.
• W2897516832 hasAuthorship W2897516832A5020763510 @default.
• W2897516832 hasAuthorship W2897516832A5024401560 @default.
• W2897516832 hasAuthorship W2897516832A5030825527 @default.
• W2897516832 hasAuthorship W2897516832A5046078938 @default.
• W2897516832 hasAuthorship W2897516832A5053512076 @default.
• W2897516832 hasAuthorship W2897516832A5053743858 @default.
• W2897516832 hasAuthorship W2897516832A5054933672 @default.
• W2897516832 hasAuthorship W2897516832A5065560361 @default.
• W2897516832 hasAuthorship W2897516832A5075539250 @default.
• W2897516832 hasAuthorship W2897516832A5078164215 @default.
• W2897516832 hasAuthorship W2897516832A5087437644 @default.
• W2897516832 hasConcept C104317684 @default.
• W2897516832 hasConcept C126322002 @default.
• W2897516832 hasConcept C127561419 @default.
• W2897516832 hasConcept C134018914 @default.
• W2897516832 hasConcept C170493617 @default.
• W2897516832 hasConcept C182704531 @default.
• W2897516832 hasConcept C185592680 @default.

• next