废气再循环1
生物
细胞生物学
转录因子
染色质免疫沉淀
基因沉默
调节器
AP-1转录因子
神经炎症
缺氧诱导因子
HIF1A型
线粒体
下调和上调
神经保护
基因敲除
粒体自噬
胶质纤维酸性蛋白
PAS域
神经科学
线粒体生物发生
基因表达调控
癌症研究
信号转导
调解人
自噬
星形胶质细胞
分子生物学
创伤性脑损伤
锌指转录因子
基因表达
认知功能衰退
作者
X Hou,Di Zhang,Xianzheng Sang,Chaogui Peng,Wen Chen,Jing Xu,Yulu Ye,Yangu Guo,Hantong Shi,Chengzi Yang,Hanzi Cai,Yijian Wang,Guangxin Chu,Haoxiang Xu,Liquan Lv,Hai Jin,Chunhui Wang,Xiaolin Qu
出处
期刊:Autophagy
[Taylor & Francis]
日期:2026-06-21
标识
DOI:10.1080/15548627.2026.2693261
摘要
Traumatic brain injury (TBI) remains a leading cause of neurological morbidity and mortality, characterized by complex pathophysiological cascades. Here, we investigate the role of the transcription factor EGR1 (early growth response 1) in modulating mitochondrial homeostasis via the HIF1A (hypoxia inducible factor 1, alpha subunit)-BNIP3 (BCL2/adenovirus E1B interacting protein 3) axis following TBI. Using integrated transcriptomic and epigenomic analyses, we identified EGR1 as a critical regulator of TBI pathology, with its expression acutely upregulated in neurons post-injury. Genetic ablation of Egr1 in mice significantly reduced neuronal apoptosis, preserved dendritic integrity, and ameliorated cognitive and sensorimotor deficits. Mechanistically, chromatin immunoprecipitation and luciferase assays revealed that EGR1 directly binds to the Hif1a promoter, repressing its transcription. Loss of EGR1 enhanced HIF1A-BNIP3-mediated mitophagy, reducing mitochondrial dysfunction and oxidative stress both in vitro and in vivo. Conversely, silencing HIF1A or BNIP3 abrogated the neuroprotective effects of EGR1 deficiency. These findings establish a novel EGR1-HIF1A-mitophagy signaling axis as a key determinant of TBI outcomes, highlighting EGR1 as a potential therapeutic target. Abbreviations: AAV: adeno-associated virus; ACTB/β-actin: actin, beta; AIF1/IBA1: allograft inflammatory factor 1; BAF: bafilomycin A1; BNIP3: BCL2/adenovirus E1B interacting protein 3; CCI: controlled cortical impact; COX8: cytochrome c oxidase subunit 8; CUT&Tag: cleavage under targets and tagmentation; DAPI: 4,’6-diamidino-2-phenylindole; DEGs: differentially expressed genes; eGFP: enhanced green fluorescent protein; EGR1: early growth response 1; GFAP: glial fibrillary acidic protein; GO: gene ontology; GSEA: gene set enrichment analysis; HCQ: hydroxychloroquine; HIF1A/HIF-1α: hypoxia inducible factor 1, alpha subunit; IGV: integrative genomics viewer; KEGG: Kyoto encyclopedia of genes and genomes; KO: knockout; LAMP1: lysosomal-associated membrane protein 1; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; Lv: lentivirus; MAP2: microtubule-associated protein 2; mCherry: monomeric cherry fluorescent protein; mRFP: monomeric red fluorescent protein; MTOR: mechanistic target of rapamycin kinase; MUT: mutant; MWM: Morris water maze; NAB1: Ngfi-A binding protein 1; NAB2: Ngfi-A binding protein 2; RBFOX3/NeuN: RNA binding protein, fox-1 homolog (C. elegans) 3; OGD: oxygen-glucose deprivation; OLIG2: oligodendrocyte transcription factor 2; PBS: phosphate-buffered saline; PECAM1/CD31: platelet/endothelial cell adhesion molecule 1; PFA: paraformaldehyde; PPI: protein-protein interaction; Puro: puromycin; ROI: region of interest; ROS: reactive oxygen species; SEM: standard error of the mean; SQSTM1/p62: sequestosome 1; TBI: traumatic brain injury; TOMM20: translocase of outer mitochondrial membrane 20; TSA: tyramide signal amplification; TUNEL: terminal deoxynucleotidyl transferase dUTP nick end labeling; VDAC1: voltage-dependent anion channel 1; WT: wild-type.
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