Kynurenic acid protects against ischemia/reperfusion injury by modulating apoptosis in cardiomyocytes
Acute myocardial infarction, often associated with ischemia/reperfusion injury (I/R), is a leading cause of death worldwide. Although the endogenous tryptophan metabolite kynurenic acid (KYNA) has been shown to exert protection against I/R injury, its mechanism of action at the cellular and molecula...
Elmentve itt :
| Szerzők: | |
|---|---|
| Dokumentumtípus: | Cikk |
| Megjelent: |
2024
|
| Sorozat: | APOPTOSIS
29 No. 9-10 |
| Tárgyszavak: | |
| doi: | 10.1007/s10495-024-02004-w |
| mtmt: | 35176616 |
| Online Access: | http://publicatio.bibl.u-szeged.hu/34429 |
| LEADER | 02533nab a2200337 i 4500 | ||
|---|---|---|---|
| 001 | publ34429 | ||
| 005 | 20241010153616.0 | ||
| 008 | 240823s2024 hu o 000 eng d | ||
| 022 | |a 1360-8185 | ||
| 024 | 7 | |a 10.1007/s10495-024-02004-w |2 doi | |
| 024 | 7 | |a 35176616 |2 mtmt | |
| 040 | |a SZTE Publicatio Repozitórium |b hun | ||
| 041 | |a eng | ||
| 100 | 1 | |a Gáspár Renáta | |
| 245 | 1 | 0 | |a Kynurenic acid protects against ischemia/reperfusion injury by modulating apoptosis in cardiomyocytes |h [elektronikus dokumentum] / |c Gáspár Renáta |
| 260 | |c 2024 | ||
| 300 | |a 1483-1498 | ||
| 490 | 0 | |a APOPTOSIS |v 29 No. 9-10 | |
| 520 | 3 | |a Acute myocardial infarction, often associated with ischemia/reperfusion injury (I/R), is a leading cause of death worldwide. Although the endogenous tryptophan metabolite kynurenic acid (KYNA) has been shown to exert protection against I/R injury, its mechanism of action at the cellular and molecular level is not well understood yet. Therefore, we examined the potential involvement of antiapoptotic mechanisms, as well as N-methyl-D-aspartate (NMDA) receptor modulation in the protective effect of KYNA in cardiac cells exposed to simulated I/R (SI/R). KYNA was shown to attenuate cell death induced by SI/R dose-dependently in H9c2 cells or primary rat cardiomyocytes. Analysis of morphological and molecular markers of apoptosis (i.e., membrane blebbing, apoptotic nuclear morphology, DNA double-strand breaks, activation of caspases) revealed considerably increased apoptotic activity in cardiac cells undergoing SI/R. The investigated apoptotic markers were substantially improved by treatment with the cytoprotective dose of KYNA. Although cardiac cells were shown to express NMDA receptors, another NMDA antagonist structurally different from KYNA was unable to protect against SI/R-induced cell death. Our findings provide evidence that the protective effect of KYNA against SI/R-induced cardiac cell injury involves antiapoptotic mechanisms, that seem to evoke independently of NMDA receptor signaling. | |
| 650 | 4 | |a Biológiai tudományok | |
| 650 | 4 | |a Klinikai orvostan | |
| 700 | 0 | 2 | |a Nógrádi-Halmi Dóra |e aut |
| 700 | 0 | 2 | |a Demján Virág |e aut |
| 700 | 0 | 2 | |a Diószegi Petra |e aut |
| 700 | 0 | 2 | |a Igaz Nóra |e aut |
| 700 | 0 | 2 | |a Vincze Anna |e aut |
| 700 | 0 | 2 | |a Pipicz Márton |e aut |
| 700 | 0 | 2 | |a Csontné Kiricsi Mónika |e aut |
| 700 | 0 | 2 | |a Vécsei László |e aut |
| 700 | 0 | 2 | |a Csont Tamás |e aut |
| 856 | 4 | 0 | |u http://publicatio.bibl.u-szeged.hu/34429/1/s10495-024-02004-w.pdf |z Dokumentum-elérés |