Hippocampal Nogo66‐NgR1 signaling activation restricts postsynaptic assembly in aged mice with postoperative neurocognitive disorders DOI Creative Commons
Min Jia,

G Li,

Chen Jiang

и другие.

Aging Cell, Год журнала: 2024, Номер unknown

Опубликована: Окт. 16, 2024

Abstract Postoperative neurocognitive disorders (pNCD) are a common neurological complication, especially in elderly following anesthesia and surgery. Yet, the underlying mechanisms of pNCD remain elusive. This study aimed to investigate molecular that compromise synaptic metaplasticity development with focus on involvement Nogo‐66 receptor 1 (NgR1) pathogenesis aged mice. Aged mice subjected laparotomy surgery exhibited anxiety‐like behavior contextual fear memory impairment. Moreover, procedure significantly increased NogoA NgR1 expressions, particularly hippocampal CA1 CA3 regions. increase led depolymerization F‐actin, attributed activation RhoA‐GTPase, resulting reduction dendritic spines changes their morphology. Additionally, these hindered efficient postsynaptic delivery subunit GluA1 GluA2 AMPA receptors (AMPARs), consequently diminishing excitatory neurotransmission hippocampus. Importantly, administering competitive antagonist peptide NEP1‐40 (Nogo‐A extracellular residues 1–40 amino acids Nogo‐66) Fasudil (a Rho‐kinase inhibitor) effectively mitigated impairments reversed deficits Our work indicates high Nogo66‐NgR1 signaling disrupts surface due F‐actin pathophysiology pNCD.

Язык: Английский

Role of dexmedetomidine in postoperative cognitive dysfunction and sleep improvement in aged rats by regulating the PI3K/Akt signaling pathway and its mechanism DOI
Ying Kong,

Xiaopeng Wang,

Jun Pang

и другие.

Brain Research, Год журнала: 2025, Номер unknown, С. 149482 - 149482

Опубликована: Янв. 1, 2025

Язык: Английский

Процитировано

1

Pharmacological inhibition of cGAS ameliorates postoperative cognitive dysfunction by suppressing caspase-3/GSDME-dependent pyroptosis DOI

Xueshan Bu,

Ping Gong, Lei Zhang

и другие.

Neurochemistry International, Год журнала: 2024, Номер 178, С. 105788 - 105788

Опубликована: Июнь 5, 2024

Язык: Английский

Процитировано

8

Unraveling the role and mechanism of mitochondria in postoperative cognitive dysfunction: a narrative review DOI Creative Commons
Zhenyong Zhang,

Wei Yang,

Lanbo Wang

и другие.

Journal of Neuroinflammation, Год журнала: 2024, Номер 21(1)

Опубликована: Ноя. 12, 2024

Abstract Postoperative cognitive dysfunction (POCD) is a frequent neurological complication encountered during the perioperative period with unclear mechanisms and no effective treatments. Recent research into pathogenesis of POCD has primarily focused on neuroinflammation, oxidative stress, changes in neural synaptic plasticity neurotransmitter imbalances. Given high-energy metabolism neurons their critical dependency mitochondria, mitochondrial directly affects neuronal function. Additionally, as primary organelles generating reactive oxygen species, mitochondria are closely linked to pathological processes neuroinflammation. Surgery anesthesia can induce dysfunction, increase disrupt quality-control via various pathways, hence serving key initiators process. We conducted review role potential postoperative by consulting relevant literature from PubMed EMBASE databases spanning past 25 years. Our findings indicate that surgery inhibit respiration, thereby reducing ATP production, decreasing membrane potential, promoting fission, inducing calcium buffering abnormalities iron accumulation, inhibiting mitophagy, increasing stress. Mitochondrial damage ultimately lead impaired function, abnormal transmission, synthesis release neurotransmitters, even death, resulting dysfunction. Targeted therapies have shown positive outcomes, holding promise novel treatment for POCD.

Язык: Английский

Процитировано

7

MEF2C Alleviates Postoperative Cognitive Dysfunction by Repressing Ferroptosis DOI Creative Commons
Shanshan Wang,

Zankai Wu,

Xueshan Bu

и другие.

CNS Neuroscience & Therapeutics, Год журнала: 2024, Номер 30(10)

Опубликована: Сен. 30, 2024

Ferroptosis, a form of programmed cell death featured by lipid peroxidation, has been proposed as potential etiology for postoperative cognitive dysfunction (POCD). Myocyte-specific enhancer factor 2C (MEF2C), transcription expressed in various brain types, implicated disorders. This study sought to ascertain whether MEF2C governs capacity affecting ferroptosis.

Язык: Английский

Процитировано

5

SNARE proteins: Core engines of membrane fusion in cancer DOI Creative Commons
Hongyi Liu,

Ruiyue Dang,

Wei Zhang

и другие.

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer, Год журнала: 2024, Номер unknown, С. 189148 - 189148

Опубликована: Июль 1, 2024

Язык: Английский

Процитировано

4

The construction of a breast cancer prognostic model by combining genes related to hypoxia and endoplasmic reticulum stress DOI
Guohua Liu, Yuan Shi, Jing Wang

и другие.

Computer Methods in Biomechanics & Biomedical Engineering, Год журнала: 2025, Номер unknown, С. 1 - 14

Опубликована: Янв. 27, 2025

Breast cancer (BC) is a malignant tumor that occurs in breast tissue. This project aims to predict the prognosis of BC patients using genes related hypoxia and endoplasmic reticulum stress (ERS). RNA-seq clinical data for were downloaded from TCGA GEO databases. Hypoxia ERS-related collected Genecards database. Univariate/multivariate Cox regression Lasso analyses used screen construct prognostic models. Patients divided into high-risk (HR) low-risk (LR) groups based on risk scores. The CIBERSORT algorithm was analyze differences immune infiltration between two groups. mutations analyzed statistically. CellMiner database drug prediction TISCH single-cell sequencing analysis. We screened 8 feature model. HR group had remarkably worse prognosis. TP53 exhibited higher mutation frequency group. analysis uncovered remarkable increase levels Macrophages M0 Tregs patients. Drug sensitivity demonstrated expression IVL greatly negatively linked with COLCHICINE. PTGS2 negative correlation Vincristine sensitivity. model can survival, status, potential drugs patients, bringing new perspective individualized treatment.

Язык: Английский

Процитировано

0

Ginsenoside 1 mitigates postoperative cognitive dysfunction by enhancing microglial Aβ clearance through the endo-lysosomal pathway DOI Creative Commons
Jing Xu, Yongchang Zhao, Gang Wang

и другие.

International Immunopharmacology, Год журнала: 2025, Номер 150, С. 114281 - 114281

Опубликована: Фев. 12, 2025

Язык: Английский

Процитировано

0

Mitophagy in perioperative neurocognitive disorder: mechanisms and therapeutic strategies DOI Creative Commons
Zhen Feng, Yan Hou, Chang Sik Yu

и другие.

European journal of medical research, Год журнала: 2025, Номер 30(1)

Опубликована: Апрель 11, 2025

Perioperative neurocognitive disorder (PND) is a common neurological complication after surgery/anesthesia in elderly patients that affect postoperative outcome and long-term quality of life, which increases the cost family social resources. The pathological mechanism PND complex not fully understood, methods prevention treatment are very limited, so it particularly important to analyze PND. Research indicates mitochondrial dysfunction pivotal initiation progression PND, although precise mechanisms remain elusive could involve disrupted mitophagy. We reviewed recent studies on link between mitophagy highlighting role key proteins abnormal discussing therapeutic strategies aimed at regulation. This provides insights into underlying potential targets.

Язык: Английский

Процитировано

0

Regulation of endoplasmic reticulum stress on autophagy and apoptosis of nucleus pulposus cells in intervertebral disc degeneration and its related mechanisms DOI Creative Commons

Jiuming Dai,

Jin Liu, Yucheng Shen

и другие.

PeerJ, Год журнала: 2024, Номер 12, С. e17212 - e17212

Опубликована: Апрель 22, 2024

Intervertebral disc degeneration (IVDD) is a common and frequent disease in orthopedics, which seriously affects the quality of life patients. Endoplasmic reticulum stress (ERS)-regulated autophagy apoptosis play an important role nucleus pulposus (NP) cells IVDD. Hypoxia serum deprivation were used to induce NP cells. Cell counting kit-8 (CCK-8) assay was detect cell activity immunofluorescence (IF) applied for appraisement glucose regulated protein 78 (GRP78) green fluorescent (GFP)-light chain 3 (LC3). detected by flow cytometry expression LC3II/I western blot. under hypoxia induced lipopolysaccharide (LPS), intervened ERS inhibitor (4-phenylbutyric acid, 4-PBA) activator (Thapsigargin, TP). Then, above functional experiments conducted again blot employed evaluation autophagy-, ERS-related proteins. Finally, stimulated LPS using z-Val-Ala-DL-Asp-fluoromethyl ketone (Z-VAD-FMK) 3-methyladenine (3-MA). CCK-8 assay, IF, performed again. Besides, levels inflammatory cytokines measured with enzyme-linked immunosorbent (ELISA) expressions programmed death markers estimated It showed that induces apoptosis. significantly activated hypoxic environment, promoted. Overall, occurrence development IVDD regulating autophagy, other death.

Язык: Английский

Процитировано

2

Neuroprotection of celastrol against postoperative cognitive dysfunction through dampening cGAS-STING signaling DOI

Xueshan Bu,

Hui Guo, Wenwei Gao

и другие.

Experimental Neurology, Год журнала: 2024, Номер 382, С. 114987 - 114987

Опубликована: Окт. 5, 2024

Язык: Английский

Процитировано

2