Matches in SemOpenAlex for { <https://semopenalex.org/work/W4386319059> ?p ?o ?g. }
- W4386319059 abstract "The canonical transient receptor potential channel (TRPC) proteins form Ca2+-permeable cation channels that are involved in various heart diseases. However, the roles of specific TRPC proteins in myocardial ischemia/reperfusion (I/R) injury remain poorly understood. We observed that TRPC1 and TRPC6 were highly expressed in the area at risk (AAR) in a coronary artery ligation induced I/R model. Trpc1−/− mice exhibited improved cardiac function, lower serum Troponin T and serum creatine kinase level, smaller infarct volume, less fibrotic scars, and fewer apoptotic cells after myocardial-I/R than wild-type or Trpc6−/− mice. Cardiomyocyte-specific knockdown of Trpc1 using adeno-associated virus 9 mitigated myocardial I/R injury. Furthermore, Trpc1 deficiency protected adult mouse ventricular myocytes (AMVMs) and HL-1 cells from death during hypoxia/reoxygenation (H/R) injury. RNA-sequencing-based transcriptome analysis revealed differential expression of genes related to reactive oxygen species (ROS) generation in Trpc1−/− cardiomyocytes. Among these genes, α-ketoglutarate dehydrogenase-like (Ogdhl) was markedly downregulated. Moreover, Trpc1 deficiency impaired the calcineurin (CaN)/nuclear factor kappa-B (NFκB) signaling pathway in AMVMs. Suppression of this pathway inhibited Ogdhl upregulation and ROS generation in HL-1 cells under H/R conditions. Chromatin Immunoprecipitation assays confirmed NFκB binding to the Ogdhl promoter. The cardioprotective effect of Trpc1 deficiency was cancelled out by overexpression of NFκB and Ogdhl in cardiomyocytes. In conclusion, our findings reveal that TRPC1 is upregulated in the AAR following myocardial I/R, leading to increased Ca2+ influx into associated cardiomyocytes. Subsequently, this upregulates Ogdhl expression through the CaN/NFκB signaling pathway, ultimately exacerbating ROS production and aggravating myocardial I/R injury." @default.
- W4386319059 created "2023-09-01" @default.
- W4386319059 creator A5008305245 @default.
- W4386319059 creator A5014896033 @default.
- W4386319059 creator A5022891823 @default.
- W4386319059 creator A5024871143 @default.
- W4386319059 creator A5047871695 @default.
- W4386319059 creator A5049301997 @default.
- W4386319059 creator A5061241145 @default.
- W4386319059 creator A5062556828 @default.
- W4386319059 creator A5064105778 @default.
- W4386319059 creator A5064267258 @default.
- W4386319059 creator A5066350349 @default.
- W4386319059 creator A5068862848 @default.
- W4386319059 creator A5071905129 @default.
- W4386319059 creator A5073667589 @default.
- W4386319059 creator A5074140059 @default.
- W4386319059 creator A5076185144 @default.
- W4386319059 creator A5078786088 @default.
- W4386319059 creator A5079882589 @default.
- W4386319059 date "2023-09-01" @default.
- W4386319059 modified "2023-10-18" @default.
- W4386319059 title "Canonical transient receptor potential channel 1 aggravates myocardial ischemia-and-reperfusion injury by upregulating reactive oxygen species" @default.
- W4386319059 cites W1485297825 @default.
- W4386319059 cites W1532684736 @default.
- W4386319059 cites W1560975206 @default.
- W4386319059 cites W1795554797 @default.
- W4386319059 cites W1930588275 @default.
- W4386319059 cites W1967411995 @default.
- W4386319059 cites W1976372232 @default.
- W4386319059 cites W1981261137 @default.
- W4386319059 cites W1986366581 @default.
- W4386319059 cites W1986866353 @default.
- W4386319059 cites W1993536160 @default.
- W4386319059 cites W1996146434 @default.
- W4386319059 cites W1999620455 @default.
- W4386319059 cites W2017726481 @default.
- W4386319059 cites W2019922945 @default.
- W4386319059 cites W2027230646 @default.
- W4386319059 cites W2028228064 @default.
- W4386319059 cites W2031943544 @default.
- W4386319059 cites W2032993608 @default.
- W4386319059 cites W2036272929 @default.
- W4386319059 cites W2044745267 @default.
- W4386319059 cites W2051788770 @default.
- W4386319059 cites W2052817643 @default.
- W4386319059 cites W2060072866 @default.
- W4386319059 cites W2084563588 @default.
- W4386319059 cites W2086667809 @default.
- W4386319059 cites W2088412949 @default.
- W4386319059 cites W2094863064 @default.
- W4386319059 cites W2097068525 @default.
- W4386319059 cites W2101354614 @default.
- W4386319059 cites W2107123744 @default.
- W4386319059 cites W2109403255 @default.
- W4386319059 cites W2112484130 @default.
- W4386319059 cites W2117041290 @default.
- W4386319059 cites W2136303393 @default.
- W4386319059 cites W2147849026 @default.
- W4386319059 cites W2156433522 @default.
- W4386319059 cites W2172683662 @default.
- W4386319059 cites W2183587606 @default.
- W4386319059 cites W2203261478 @default.
- W4386319059 cites W2253619901 @default.
- W4386319059 cites W2469730409 @default.
- W4386319059 cites W2614016715 @default.
- W4386319059 cites W2614269530 @default.
- W4386319059 cites W2616481231 @default.
- W4386319059 cites W2619658153 @default.
- W4386319059 cites W2755709159 @default.
- W4386319059 cites W2759278862 @default.
- W4386319059 cites W2793830108 @default.
- W4386319059 cites W2801190461 @default.
- W4386319059 cites W2802360440 @default.
- W4386319059 cites W2824108843 @default.
- W4386319059 cites W2897211070 @default.
- W4386319059 cites W2899981476 @default.
- W4386319059 cites W2900089054 @default.
- W4386319059 cites W2902325019 @default.
- W4386319059 cites W2908439034 @default.
- W4386319059 cites W2919777598 @default.
- W4386319059 cites W2922045413 @default.
- W4386319059 cites W2940468863 @default.
- W4386319059 cites W2998625923 @default.
- W4386319059 cites W3007985981 @default.
- W4386319059 cites W3009940069 @default.
- W4386319059 cites W3011459566 @default.
- W4386319059 cites W3034236107 @default.
- W4386319059 cites W3038341522 @default.
- W4386319059 cites W3080530762 @default.
- W4386319059 cites W3131208881 @default.
- W4386319059 cites W3174747352 @default.
- W4386319059 cites W4225755310 @default.
- W4386319059 cites W4230078341 @default.
- W4386319059 cites W4280653683 @default.
- W4386319059 cites W4310576965 @default.
- W4386319059 doi "https://doi.org/10.1016/j.jpha.2023.08.018" @default.
- W4386319059 hasPublicationYear "2023" @default.
- W4386319059 type Work @default.
- W4386319059 citedByCount "0" @default.