FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2908203321> ?p ?o ?g. }

• W2908203321 endingPage "50" @default.
• W2908203321 startingPage "38" @default.
• W2908203321 abstract "LonP1 is an essential mitochondrial protease, which is crucial for maintaining mitochondrial proteostasis and mitigating cell stress. However, the importance of LonP1 during cardiac stress is largely unknown.To determine the functions of LonP1 during ischemia/reperfusion (I/R) injury in vivo, and hypoxia-reoxygenation (H/R) stress in vitro.LonP1 was induced 2-fold in wild-type mice during cardiac ischemic preconditioning (IPC), which protected the heart against ischemia-reperfusion (I/R) injury. In contrast, haploinsufficiency of LonP1 (LONP1+/-) abrogated IPC-mediated cardioprotection. Furthermore, LONP1+/- mice showed significantly increased infarct size after I/R injury, whereas mice with 3-4 fold cardiac-specific overexpression of LonP1 (LonTg) had substantially smaller infarct size and reduced apoptosis compared to wild-type controls. To investigate the mechanisms underlying cardioprotection, LonTg mice were subjected to ischemia (45 min) followed by short intervals of reperfusion (10, 30, 120 min). During early reperfusion, the left ventricles of LonTg mice showed substantially reduced oxidative protein damage, maintained mitochondrial redox homeostasis, and showed a marked downregulation of both Complex I protein level and activity in contrast to NTg mice. Conversely, when LonP1 was knocked down in isolated neonatal rat ventricular myocytes (NRVMs), an up-regulation of Complex I subunits and electron transport chain (ETC) activities was observed, which was associated with increased superoxide production and reduced respiratory efficiency. The knockdown of LonP1 in NRVMs caused a striking dysmorphology of the mitochondrial inner membrane, mitochondrial hyperpolarization and increased hypoxia-reoxygenation (H/R)-activated apoptosis. Whereas, LonP1 overexpression blocked H/R-induced cell death.LonP1 is an endogenous mediator of cardioprotection. Our findings show that upregulation of LonP1 mitigates cardiac injury by preventing oxidative damage of proteins and lipids, preserving mitochondrial redox balance and reprogramming bioenergetics by reducing Complex I content and activity. Mechanisms that promote the upregulation of LonP1 could be beneficial in protecting the myocardium from cardiac stress and limiting I/R injury." @default.
• W2908203321 created "2019-01-11" @default.
• W2908203321 creator A5001378257 @default.
• W2908203321 creator A5002791625 @default.
• W2908203321 creator A5037804491 @default.
• W2908203321 creator A5041077824 @default.
• W2908203321 creator A5043143669 @default.
• W2908203321 creator A5066819711 @default.
• W2908203321 creator A5068159646 @default.
• W2908203321 creator A5071213647 @default.
• W2908203321 creator A5075261929 @default.
• W2908203321 creator A5086160044 @default.
• W2908203321 creator A5087974982 @default.
• W2908203321 creator A5091705107 @default.
• W2908203321 date "2019-03-01" @default.
• W2908203321 modified "2023-10-18" @default.
• W2908203321 title "Mitochondrial LonP1 protects cardiomyocytes from ischemia/reperfusion injury in vivo" @default.
• W2908203321 cites W1583148430 @default.
• W2908203321 cites W1965091767 @default.
• W2908203321 cites W1965297825 @default.
• W2908203321 cites W1968698003 @default.
• W2908203321 cites W1981257887 @default.
• W2908203321 cites W1998162530 @default.
• W2908203321 cites W2000770940 @default.
• W2908203321 cites W2000800148 @default.
• W2908203321 cites W2004147608 @default.
• W2908203321 cites W2006118708 @default.
• W2908203321 cites W2007280799 @default.
• W2908203321 cites W2007577648 @default.
• W2908203321 cites W2009595653 @default.
• W2908203321 cites W2017228519 @default.
• W2908203321 cites W2026525843 @default.
• W2908203321 cites W2028717822 @default.
• W2908203321 cites W2029704497 @default.
• W2908203321 cites W2036284918 @default.
• W2908203321 cites W2036997218 @default.
• W2908203321 cites W2040725645 @default.
• W2908203321 cites W2042921983 @default.
• W2908203321 cites W2043355876 @default.
• W2908203321 cites W2043395636 @default.
• W2908203321 cites W2051395985 @default.
• W2908203321 cites W2051551158 @default.
• W2908203321 cites W2054987125 @default.
• W2908203321 cites W2062742764 @default.
• W2908203321 cites W2069134915 @default.
• W2908203321 cites W2070433264 @default.
• W2908203321 cites W2075308841 @default.
• W2908203321 cites W2078704533 @default.
• W2908203321 cites W2089870625 @default.
• W2908203321 cites W2097668381 @default.
• W2908203321 cites W2110649328 @default.
• W2908203321 cites W2121594663 @default.
• W2908203321 cites W2122091775 @default.
• W2908203321 cites W2126252005 @default.
• W2908203321 cites W2131538613 @default.
• W2908203321 cites W2143505819 @default.
• W2908203321 cites W2146217294 @default.
• W2908203321 cites W2148658873 @default.
• W2908203321 cites W2176998809 @default.
• W2908203321 cites W2226472011 @default.
• W2908203321 cites W2239083587 @default.
• W2908203321 cites W2281735941 @default.
• W2908203321 cites W2346097989 @default.
• W2908203321 cites W2465744647 @default.
• W2908203321 cites W2555272644 @default.
• W2908203321 cites W2560581736 @default.
• W2908203321 cites W2606866555 @default.
• W2908203321 cites W2888883335 @default.
• W2908203321 doi "https://doi.org/10.1016/j.yjmcc.2018.12.017" @default.
• W2908203321 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30625302" @default.
• W2908203321 hasPublicationYear "2019" @default.
• W2908203321 type Work @default.
• W2908203321 sameAs 2908203321 @default.
• W2908203321 citedByCount "50" @default.
• W2908203321 countsByYear W29082033212019 @default.
• W2908203321 countsByYear W29082033212020 @default.
• W2908203321 countsByYear W29082033212021 @default.
• W2908203321 countsByYear W29082033212022 @default.
• W2908203321 countsByYear W29082033212023 @default.
• W2908203321 crossrefType "journal-article" @default.
• W2908203321 hasAuthorship W2908203321A5001378257 @default.
• W2908203321 hasAuthorship W2908203321A5002791625 @default.
• W2908203321 hasAuthorship W2908203321A5037804491 @default.
• W2908203321 hasAuthorship W2908203321A5041077824 @default.
• W2908203321 hasAuthorship W2908203321A5043143669 @default.
• W2908203321 hasAuthorship W2908203321A5066819711 @default.
• W2908203321 hasAuthorship W2908203321A5068159646 @default.
• W2908203321 hasAuthorship W2908203321A5071213647 @default.
• W2908203321 hasAuthorship W2908203321A5075261929 @default.
• W2908203321 hasAuthorship W2908203321A5086160044 @default.
• W2908203321 hasAuthorship W2908203321A5087974982 @default.
• W2908203321 hasAuthorship W2908203321A5091705107 @default.
• W2908203321 hasBestOaLocation W29082033212 @default.
• W2908203321 hasConcept C126322002 @default.
• W2908203321 hasConcept C2779676291 @default.
• W2908203321 hasConcept C28859421 @default.
• W2908203321 hasConcept C541997718 @default.
• W2908203321 hasConcept C71924100 @default.

• next