Iron overload enhances TBI-induced cardiac dysfunction by promoting ferroptosis and cardiac inflammation
Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved..
Previous studies have proved that cardiac dysfunction and myocardial damage can be found in TBI patients, but the underlying mechanisms of myocardial damage induced by TBI can't be illustrated. We want to investigate the function of ferroptosis in myocardial damage after TBI and determine if inhibiting iron overload might lessen myocardial injury after TBI due to the involvement of iron overload in the process of ferroptosis and inflammation. We detect the expression of ferroptosis-related proteins in cardiac tissue at different time points after TBI, indicating that TBI can cause ferroptosis in the heart in vivo. The echocardiography and myocardial enzymes results showed that ferroptosis can aggravate TBI-induced cardiac dysfunction. The result of DHE staining and 4-HNE expression showed that inhibition of ferroptosis can reduce ROS production and lipid peroxidation in myocardial tissue. In further experiments, DFO intervention was used to explore the effect of iron overload inhibition on myocardial ferroptosis after TBI, the production of ROS, expression of p38 MAPK and NF-κB was detected to explore the effect of iron overload on myocardial inflammation after TBI. The results above show that TBI can cause heart ferroptosis in vivo. Inhibition of iron overload can alleviate myocardial injury after TBI by reducing ferroptosis and inflammatory response induced by TBI.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2023 |
|---|---|
| Erschienen: |
2023 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:682 |
|---|---|
| Enthalten in: |
Biochemical and biophysical research communications - 682(2023) vom: 19. Nov., Seite 46-55 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Peng, Ruilong [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Ferroptosis |
|---|
| Anmerkungen: |
Date Completed 01.11.2023 Date Revised 05.11.2023 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1016/j.bbrc.2023.09.088 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM362955972 |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM362955972 | ||
| 003 | DE-627 | ||
| 005 | 20231226092324.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2023 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.bbrc.2023.09.088 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1209.xml |
| 035 | |a (DE-627)NLM362955972 | ||
| 035 | |a (NLM)37801989 | ||
| 035 | |a (PII)S0006-291X(23)01130-0 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Peng, Ruilong |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Iron overload enhances TBI-induced cardiac dysfunction by promoting ferroptosis and cardiac inflammation |
| 264 | 1 | |c 2023 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 01.11.2023 | ||
| 500 | |a Date Revised 05.11.2023 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a Copyright © 2023 The Authors. Published by Elsevier Inc. All rights reserved. | ||
| 520 | |a Previous studies have proved that cardiac dysfunction and myocardial damage can be found in TBI patients, but the underlying mechanisms of myocardial damage induced by TBI can't be illustrated. We want to investigate the function of ferroptosis in myocardial damage after TBI and determine if inhibiting iron overload might lessen myocardial injury after TBI due to the involvement of iron overload in the process of ferroptosis and inflammation. We detect the expression of ferroptosis-related proteins in cardiac tissue at different time points after TBI, indicating that TBI can cause ferroptosis in the heart in vivo. The echocardiography and myocardial enzymes results showed that ferroptosis can aggravate TBI-induced cardiac dysfunction. The result of DHE staining and 4-HNE expression showed that inhibition of ferroptosis can reduce ROS production and lipid peroxidation in myocardial tissue. In further experiments, DFO intervention was used to explore the effect of iron overload inhibition on myocardial ferroptosis after TBI, the production of ROS, expression of p38 MAPK and NF-κB was detected to explore the effect of iron overload on myocardial inflammation after TBI. The results above show that TBI can cause heart ferroptosis in vivo. Inhibition of iron overload can alleviate myocardial injury after TBI by reducing ferroptosis and inflammatory response induced by TBI | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Ferroptosis | |
| 650 | 4 | |a Inflammation | |
| 650 | 4 | |a Iron overload | |
| 650 | 4 | |a TBI | |
| 650 | 7 | |a Reactive Oxygen Species |2 NLM | |
| 700 | 1 | |a Liu, Xilei |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Cong |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Fanjian |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Tuo |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Lei |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Hejun |e verfasserin |4 aut | |
| 700 | 1 | |a Gao, Yalong |e verfasserin |4 aut | |
| 700 | 1 | |a Yu, Xuefang |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Shu |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Jianning |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Biochemical and biophysical research communications |d 1960 |g 682(2023) vom: 19. Nov., Seite 46-55 |w (DE-627)NLM000000035 |x 1090-2104 |7 nnns |
| 773 | 1 | 8 | |g volume:682 |g year:2023 |g day:19 |g month:11 |g pages:46-55 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1016/j.bbrc.2023.09.088 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 682 |j 2023 |b 19 |c 11 |h 46-55 | ||