Many studies in the open literature have highlighted the critical roles of endoplasmic reticulum stress and ferroptosis in neurological diseases such as neurodegenerative diseases, brain injuries, and depression, indicating that they are involved in the onset and progression of these diseases. Therefore, it is essential to explore the regulatory mechanisms and potential interventions targeting endoplasmic reticulum stress and ferroptosis in neurological diseases. However, most existing research has primarily focused on the unidirectional mechanisms of endoplasmic reticulum stress and ferroptosis within the nervous system, with a lack of in-depth investigations into their interactions. In this paper, we first present an overview of the pathogenesis of endoplasmic reticulum stress and ferroptosis, along with their roles in neurological diseases. We then summarize the latest findings on the interaction mechanism between endoplasmic reticulum stress and ferroptosis from the perspectives of calcium iron homeostasis, reactive oxygen species, microenvironment, and related factors. Finally, we explore the potential molecular mechanisms and targeted interventions associated with endoplasmic reticulum stress and ferroptosis in neurological diseases.
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http://dx.doi.org/10.1007/s11064-025-04348-4 | DOI Listing |
J Ethnopharmacol
March 2025
School of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, Nanjing, 210023, China. Electronic address:
Ethnopharmacological Relevance: Zhizichi Decoction (ZZCD), a traditional Chinese medicine (TCM), is derived from the combination of Gardenia jasminoides J.Ellis [Rubiaceae] and Semen Sojae Praeparatum, a fermented derivative of Glycine max (L.) Merr.
View Article and Find Full Text PDFProg Lipid Res
March 2025
Department of Biochemistry, Kagawa University School of Medicine, 1750-1 Ikenobe, Miki, Kagawa 761-0793, Japan. Electronic address:
The phospholipase A and acyltransferase (PLAAT) family is a group of structurally related proteins that are conserved among vertebrates. In humans, the family comprises five members (PLAAT1-5), which share common domain structures, and functions as phospholipase A/A and acyltransferase enzymes. Regarding acyltransferase activities, PLAATs produce N-acyl-phosphatidylethanolamines, which serve as the precursor of bioactive N-acylethanolamines (NAEs).
View Article and Find Full Text PDFJ Biol Chem
March 2025
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, PA, USA. Electronic address:
The potassium chloride co-transporter 2 (KCC2) is required for neuronal development, and KCC2 dysregulation is implicated in several neurodevelopmental disorders, including schizophrenia, autism, and epilepsy. A dozen mutations in the KCC2-encoding gene, SLC12A5, are associated with these disorders, but few are fully characterized. To this end, we examined KCC2 biogenesis in a HEK293 cell model.
View Article and Find Full Text PDFFood Chem Toxicol
March 2025
Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin, Heilongjiang 150081, China; Key Lab of Etiology and Epidemiology, Education Bureau of Heilongjiang Province & Ministry of Health (23618504), Harbin Medical University, Harbin 150081, China; Heilongjiang Provincial Key Lab of Trace Elements and Human Health Harbin Medical University, Harbin 150081, China. Electronic address:
Long-term fluoride exposure can produce neurotoxicity. Anthocyanins, as antioxidants, have a certain protective effect in nerve damage. This study aimed to investigate the protective role of anthocyanins in fluoride-induced neurological damage due to endoplasmic reticulum stress (ERS).
View Article and Find Full Text PDFMol Metab
March 2025
Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA; Howard Hughes Medical Institute, Dallas, TX, 75390, USA; Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA. Electronic address:
The bi-functional enzyme FicD catalyzes AMPylation and deAMPylation of the endoplasmic reticulum chaperone BiP to modulate ER homeostasis and the unfolded protein response (UPR). Human hFicD with an arginine-to-serine mutation disrupts FicD deAMPylation activity resulting in severe neonatal diabetes. We generated the mFicD mutation in mice to create a pre-clinical murine model for neonatal diabetes.
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