FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2109736486> ?p ?o ?g. }

• W2109736486 abstract "Abstract Background Endoplasmic reticulum (ER) stress is considered one of the mechanisms contributing to reactive oxygen species (ROS)- mediated cell apoptosis. In diabetic cardiomyopathy (DCM), cell apoptosis is generally accepted as the etiological factor and closely related to cardiac ROS generation. ER stress is proposed the link between ROS and cell apoptosis; however, the signaling pathways and their roles in participating ER stress- induced apoptosis in DCM are still unclear. Methods In this study, we investigated the signaling transductions in ROS- dependent ER stress- induced cardiomocyte apoptosis in animal model of DCM. Moreover, in order to clarify the roles of IRE1 (inositol - requiring enzyme-1), PERK (protein kinase RNA (PKR)- like ER kinase) and ATF6 (activating transcription factor-6) in conducting apoptotic signal in ROS- dependent ER stress- induced cardiomocyte apoptosis, we further investigated apoptosis in high- glucose incubated cardiomyocytes with IRE1, ATF6 and PERK- knocked down respectively. Results we demonstrated that the ER stress sensors, referred as PERK, IRE1 and ATF6, were activated in ROS- mediated ER stress- induced cell apoptosis in rat model of DCM which was characterized by cardiac pump and electrical dysfunctions. The deletion of PERK in myocytes exhibited stronger protective effect against apoptosis induced by high- glucose incubation than deletion of ATF6 or IRE in the same myocytes. By subcellular fractionation, rather than ATF6 and IRE1, in primary cardiomyocytes, PERK was found a component of MAMs (mitochondria-associated endoplasmic reticulum membranes) which was the functional and physical contact site between ER and mitochondria. Conclusions ROS- stimulated activation of PERK signaling pathway takes the major responsibility rather than IRE1 or ATF6 signaling pathways in ROS- medicated ER stress- induced myocyte apoptosis in DCM." @default.
• W2109736486 created "2016-06-24" @default.
• W2109736486 creator A5003019825 @default.
• W2109736486 creator A5011504948 @default.
• W2109736486 creator A5017383224 @default.
• W2109736486 creator A5075149036 @default.
• W2109736486 creator A5078333667 @default.
• W2109736486 creator A5078576975 @default.
• W2109736486 creator A5083984738 @default.
• W2109736486 date "2013-11-02" @default.
• W2109736486 modified "2023-10-15" @default.
• W2109736486 title "Protein kinase RNA- like endoplasmic reticulum kinase (PERK) signaling pathway plays a major role in reactive oxygen species (ROS)- mediated endoplasmic reticulum stress- induced apoptosis in diabetic cardiomyopathy" @default.
• W2109736486 cites W1963568186 @default.
• W2109736486 cites W1965872874 @default.
• W2109736486 cites W1970504457 @default.
• W2109736486 cites W1973531470 @default.
• W2109736486 cites W1976943917 @default.
• W2109736486 cites W1978854975 @default.
• W2109736486 cites W1982204392 @default.
• W2109736486 cites W1983640724 @default.
• W2109736486 cites W1986199468 @default.
• W2109736486 cites W1987001379 @default.
• W2109736486 cites W1989352421 @default.
• W2109736486 cites W1992564227 @default.
• W2109736486 cites W1996407657 @default.
• W2109736486 cites W1998300009 @default.
• W2109736486 cites W2005944283 @default.
• W2109736486 cites W2016009699 @default.
• W2109736486 cites W2020457477 @default.
• W2109736486 cites W2022265177 @default.
• W2109736486 cites W2025186700 @default.
• W2109736486 cites W2025511820 @default.
• W2109736486 cites W2027364427 @default.
• W2109736486 cites W2028765929 @default.
• W2109736486 cites W2031484324 @default.
• W2109736486 cites W2034213169 @default.
• W2109736486 cites W2036557271 @default.
• W2109736486 cites W2052622892 @default.
• W2109736486 cites W2054005523 @default.
• W2109736486 cites W2055143260 @default.
• W2109736486 cites W2057835131 @default.
• W2109736486 cites W2060574598 @default.
• W2109736486 cites W2064331279 @default.
• W2109736486 cites W2067240761 @default.
• W2109736486 cites W2069136548 @default.
• W2109736486 cites W2070647639 @default.
• W2109736486 cites W2077807148 @default.
• W2109736486 cites W2078265535 @default.
• W2109736486 cites W2081731224 @default.
• W2109736486 cites W2082171506 @default.
• W2109736486 cites W2082315075 @default.
• W2109736486 cites W2083278580 @default.
• W2109736486 cites W2089198803 @default.
• W2109736486 cites W2091133442 @default.
• W2109736486 cites W2100347985 @default.
• W2109736486 cites W2102730253 @default.
• W2109736486 cites W2108209027 @default.
• W2109736486 cites W2115205812 @default.
• W2109736486 cites W2119801354 @default.
• W2109736486 cites W2120054003 @default.
• W2109736486 cites W2126706756 @default.
• W2109736486 cites W2127639686 @default.
• W2109736486 cites W2131073646 @default.
• W2109736486 cites W2132699009 @default.
• W2109736486 cites W2133277178 @default.
• W2109736486 cites W2133644385 @default.
• W2109736486 cites W2139684004 @default.
• W2109736486 cites W2144036883 @default.
• W2109736486 cites W2145487661 @default.
• W2109736486 cites W2145592978 @default.
• W2109736486 cites W2147802824 @default.
• W2109736486 cites W2151565739 @default.
• W2109736486 cites W2153139917 @default.
• W2109736486 cites W2153292251 @default.
• W2109736486 cites W2156604564 @default.
• W2109736486 cites W2161421542 @default.
• W2109736486 cites W2165832533 @default.
• W2109736486 cites W2396310886 @default.
• W2109736486 cites W2471605942 @default.
• W2109736486 doi "https://doi.org/10.1186/1475-2840-12-158" @default.
• W2109736486 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4176998" @default.
• W2109736486 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/24180212" @default.
• W2109736486 hasPublicationYear "2013" @default.
• W2109736486 type Work @default.
• W2109736486 sameAs 2109736486 @default.
• W2109736486 citedByCount "160" @default.
• W2109736486 countsByYear W21097364862014 @default.
• W2109736486 countsByYear W21097364862015 @default.
• W2109736486 countsByYear W21097364862016 @default.
• W2109736486 countsByYear W21097364862017 @default.
• W2109736486 countsByYear W21097364862018 @default.
• W2109736486 countsByYear W21097364862019 @default.
• W2109736486 countsByYear W21097364862020 @default.
• W2109736486 countsByYear W21097364862021 @default.
• W2109736486 countsByYear W21097364862022 @default.
• W2109736486 countsByYear W21097364862023 @default.
• W2109736486 crossrefType "journal-article" @default.
• W2109736486 hasAuthorship W2109736486A5003019825 @default.
• W2109736486 hasAuthorship W2109736486A5011504948 @default.
• W2109736486 hasAuthorship W2109736486A5017383224 @default.

• next