TRPM7 mediates endoplasmic reticulum stress and ferroptosis in sepsis-induced myocardial injury

Deng, Wen; Ren, Guobin; Luo, Jiajing; Gao, Shan; Huang, Wenyuan; Liu, Weitao; Ye, Shupei

doi:10.1007/s10863-023-09968-5

Cited by 3 publications

(1 citation statement)

References 35 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Notably, inhibition of TRPM7 also reduced articular cartilage destruction and suppressed chondrocyte ferroptosis in adjuvant arthritis rats (AAR). This is achieved by reducing intracellular Ca 2+ overload through inhibition of TRPM7, which in turn reduces calcium-activated protein kinase Cα (PKCα)/NOX4 pathway-mediated ROS production, thus attenuating cellular ferroptosis and ERS ( 94 , 95 ).…”

Section: Relationship Between Ers and Ferroptosis: A Potential New Di...mentioning

confidence: 99%

Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

Ao,

Hu,

Huang

2024

Front. Immunol.

View full text Add to dashboard Cite

Ferroptosis is an iron-dependent mode of cell death distinct from apoptosis and necrosis. Its mechanisms mainly involve disordered iron metabolism, lipid peroxide deposition, and an imbalance of the antioxidant system. The endoplasmic reticulum is an organelle responsible for protein folding, lipid metabolism, and Ca2+ regulation in cells. It can be induced to undergo endoplasmic reticulum stress in response to inflammation, oxidative stress, and hypoxia, thereby regulating intracellular environmental homeostasis through unfolded protein responses. It has been reported that ferroptosis and endoplasmic reticulum stress (ERS) have an interaction pathway and jointly regulate cell survival and death. Both have also been reported separately in rheumatoid arthritis (RA) mechanism studies. However, studies on the correlation between ferroptosis and ERS in RA have not been reported so far. Therefore, this paper reviews the current status of studies and the potential correlation between ferroptosis and ERS in RA, aiming to provide a research reference for developing treatments for RA.

show abstract

Section: Relationship Between Ers and Ferroptosis: A Potential New Di...mentioning

confidence: 99%

Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

Ao,

Hu,

Huang

2024

Front. Immunol.

View full text Add to dashboard Cite

show abstract

METTL14 Promotes Lipopolysaccharide-Induced Myocardial Damage via m6A-Dependent Stabilization of TRPM7 mRNA

Wu,

Huang,

Xiao

et al. 2024

Int. Heart J.

View full text Add to dashboard Cite

Mild therapeutic hypothermic protection activates the PI3K/AKT signaling pathway to inhibit TRPM7 and suppress ferroptosis induced by myocardial ischemia‑reperfusion injury

Li,

Chen,

et al. 2024

Mol Med Rep

View full text Add to dashboard Cite

The present study aimed to investigate the role of PI3K-mediated ferroptosis signaling induced by mild therapeutic hypothermia (MTH), which was defined as a temperature of 34°C, in protecting against myocardial ischemia-reperfusion (I/R) injury (MIRI). To meet this aim, H9C2 cells underwent hypoxia-reperfusion (H/R) and/or MTH. The MTT assay was used to assess cell viability, cytotoxicity was measured using a lactate dehydrogenase cytotoxicity assay, and Annexin V-FITC/PI flow cytometric analysis was used to analyze early and late cell apoptosis. In addition, 84 healthy adult male Sprague-Dawley rats were randomly divided into seven groups (n=12), and underwent I/R and various treatments. Hemodynamics were monitored, and the levels of myocardial injury marker enzymes and oxidative stress markers in myocardial tissue were measured using ELISA. The expression levels of PI3K, AKT, transient receptor potential cation channel subfamily M member 7 (TRPM7), glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long chain family member 4 (ACSL4) in animals and cells were measured using western blot analysis. These experiments revealed that MTH could effectively reduce myocardial infarct size, improve hemodynamic performance following MIRI and suppress myocardial apoptosis, thereby contributing to the recovery from H/R injury. Mechanistically, MTH was revealed to be able to activate the PI3K/AKT signaling pathway in cells, upregulating GPX4, and downregulating the expression levels of TRPM7 and ACSL4. Treatment with 2-aminoethoxydiphenyl borate (an inhibitor of TRPM7) could further strengthen the myocardial protective effects of MTH, whereas treatment with erastin (promoter of ferroptosis) and wortmannin (inhibitor of PI3K) led to the effective elimination of the myocardial protective effects of MTH. Compared with in the I/R group, the PI3K/AKT activation level and the expression levels of GPX4 were both significantly increased, whereas the expression levels of TRPM7 and ACSL4 were significantly decreased in the I/R + MTH group. Taken together, the results of the present study indicated that MTH may activate the PI3K/AKT signaling pathway to inhibit TRPM7 and suppress ferroptosis induced by MIRI.

show abstract

TRPM7 mediates endoplasmic reticulum stress and ferroptosis in sepsis-induced myocardial injury

Cited by 3 publications

References 35 publications

Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

Ferroptosis and endoplasmic reticulum stress in rheumatoid arthritis

METTL14 Promotes Lipopolysaccharide-Induced Myocardial Damage via m6A-Dependent Stabilization of TRPM7 mRNA

Mild therapeutic hypothermic protection activates the PI3K/AKT signaling pathway to inhibit TRPM7 and suppress ferroptosis induced by myocardial ischemia‑reperfusion injury

Contact Info

Product

Resources

About