JOURNAL OF BIOENERGETICS AND BIOMEMBRANES生物能量学与生物膜杂志
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES(英文缩写 J BIOENERG BIOMEMBR),ISSN 0145-479X,eISSN 1573-6881,中文译名:生物能量学与生物膜杂志 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-11-01 至 2026-10-31，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 3.853 | Q2 |
| 2022 | 3.000 | Q2 |
| 2023 | 2.900 | Q2 |
| 2024 | 3.000 | Q2 |
| 2025 | 3.700 | Q2 |
JOURNAL OF BIOENERGETICS AND BIOMEMBRANES 最新收录文献
-
1. M2-Exo-derived miR-1227-5p protects against periodontitis through inhibiting USP2-dependent deubiquitination of Drp1.
1. M2-Exo来源的miR-1227-5p通过抑制USP2依赖的Drp1去泛素化来预防牙周炎PMID:日期:2026-09-24Periodontitis is a common chronic inflammatory disease with an exaggerated host immune response. M2 type macrophages exert protective properties in periodontitis. This study aimed to investigate the role of M2-Exo-derived miR-1227-5p in periodontitis. M2-Exo were verified using TEM and NTR assay. miRNA and mRNA levels were determined using RT-qPCR. periodontal ligament stem cells (PDLCs) were exposed to LPS in establish in vitro periodontitis model. Gene expression was determined using Western blot and immunofluorescence. The binding sites of miR-1227-5p on USP2 were predicted by TargetScan and verified by luciferase, RNA pull-down, and RIP assays. Deubiquitination of Drp1 was determined using in vitro ubiquitination assay. Cellular behaviors of PDLCs were analyzed by CCK-8, alizarin red staining, and ALP staining. LPS exposure induced mitochondrial dysfunction and suppressed the osteogenesis of PDLCs. M2-Exo-derived miR-1227-5p improved mitochondrial function and promoted the proliferation and osteogenesis of PDLCs. miR-1227-5p directly targeted USP2. USP2 overexpression reversed the effects of miR-1227-5p and improved mitochondrial function and the osteogenesis of PDLCs. Moreover, miR-1227-5p targeted USP2 to inhibit the deubiquitination of Drp1, improving mitochondrial function. Furthermore, M2-Exo-derived miR-1227-5p alleviates periodontitis via regulating USP2/Drp1. Therefore, M2-Exo hold great potential for future clinical applications.
-
2. Integrated bioinformatics analysis, machine learning, and experimental validation reveal that ACSL1 drives myocardial ischemia reperfusion injury via ferroptosis.
2. 综合生物信息学分析、机器学习和实验验证揭示ACSL1通过铁死亡驱动心肌缺血再灌注损伤PMID:日期:2026-09-24Myocardial ischemia-reperfusion injury (MIRI) is a significant factor in the development of cardiac dysfunction following an acute myocardial infarction (AMI). Ferroptosis, a type of regulated cell death driven by iron and marked by lipid peroxidation, has attracted increasing attention for its pivotal role in the pathogenesis of MIRI. It has been reported that acyl-CoA synthetase long chain family member 1 (ACSL1), a ferroptosis promoter, could mediate ferroptosis of myocardial cells during AMI. However, the specific function and mechanism of ACSL1 in AMI are still unclear. Differentially expressed genes in AMI were identified from the Gene Expression Omnibus (GEO) databases (GSE166780 and GSE97320), and ferroptosis-related genes were acquired from the PathCards database. Through integrated analysis of the two genomes, ferroptosis-related genes in AMI were identified. Then, the identified genes were subjected to cross-validation using three machine learning algorithms (LASSO, SVM-RFE, and RF), ultimately identifying characteristic genes. ACSL1, Forkhead box protein O4 (FOXO4), tripartite motif-containing protein 25 (TRIM25), and GPX4 protein levels were detected using western blot. Cell viability and apoptosis were Cell Counting Kit-8 (CCK-8) and flow cytometry. Interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) levels were analyzed using enzyme-linked immunosorbent assay (ELISA). Fe2+ level, lipid reactive oxygen species (ROS) level, and GSH level were examined using commercial kits. Flow cytometric analysis of mitochondrial membrane potential using JC-1. Binding between FOXO4 and ACSL1 promoter was predicted by JASPAR and verified using dual-luciferase reporter and ChIP assays. The stability of ACSL1 was assessed by CHX assay. Interaction between TRIM25 and ACSL1 was verified using Co-immunoprecipitation (CoIP) assay. The effect of ACSL1 on myocardial injury was detected using a mouse MIR model. After screening and identification, ferroptosis-related gene ACSL1 in AMI was selected for this study. ACSL1 expression was increased in AMI patients and Ischemia/Reperfusion (H/R)-treated AC16 cells. H/R-triggered AC16 cell viability inhibition, and apoptosis, inflammatory response, ferroptosis, and mitochondrial dysfunction promotion were partly abolished by ACSL1 silencing. Mechanistically, FOXO4 activated ACSL1 transcription by binding to its promoter region. TRIM25 facilitated ACSL1 ubiquitination and decreased its protein stability. ACSL1 downregulation could relieve myocardial damage in vivo. ACSL1 was identified as a key ferroptosis-related gene in AMI. Furthermore, FOXO4-activated transcription and TRIM25-mediated ubiquitination-dependent degradation of ACSL1 could affect H/R-induced cardiomyocyte damage and ferroptosis, providing a promising therapeutic target for MIRI treatment.
-
3. FTO-mediated GPX4 m6A modification in ferroptosis-induced DNA damage and inflammatory response during acute lung injury.
3. FTO介导的GPX4 m6A修饰在急性肺损伤中铁死亡诱导的DNA损伤和炎症反应中的作用PMID:日期:2026-09-16To investigate the role of Fat Mass and Obesity-associated Protein (FTO) in acute lung injury (ALI) and elucidate how it regulates ferroptosis via N6-methyladenosine (m6A) modification of glutathione peroxidase 4 (GPX4). ALI models were established in LPS‑stimulated BEAS‑2B cells and mice. FTO expression was modulated by siRNA, inhibitors, or adeno‑associated virus. Ferroptosis, apoptosis, inflammation and DNA damage were assessed by RIP‑qPCR, meRIP‑qPCR, Western blotting and TEM. GPX4 m6A site mutants were constructed. GPX4 mRNA/protein stability and translation were analyzed using actinomycin D and cycloheximide. Establish an LPS-induced ALI mouse model, perform adeno-associated viral knockdown of FTO in lung tissue, and validate in vivo using GPX4 inhibitors. FTO inhibition significantly attenuated LPS-induced ferroptosis, apoptosis, inflammatory responses, and mitochondrial damage. Mechanistically, FTO accelerates GPX4 protein degradation by reducing m6A modification of GPX4, thereby downregulating GPX4 protein expression in a post-transcriptional and post-translational manner. This leads to intracellular iron accumulation, ROS bursts, lipid peroxidation, and DNA damage. Mutating the m6A site in GPX4 or supplementing GPX4 protein effectively reverses the aforementioned damage. Silencing FTO in vivo significantly ameliorates pulmonary tissue pathology, impaired lung function, ferroptosis, and inflammatory responses in mice via a GPX4-dependent pathway, whereas GPX4 inhibition reverses this protective effect. FTO exacerbates ALI by mediating m6A modification of GPX4 and downregulates its protein expression, thereby driving ferroptosis and DNA damage. Targeting the FTO-GPX4 axis may offer novel therapeutic strategies for ALI.
-
4. Mitokines as bioenergetic stress signals in cardiovascular disease: mitochondrial communication, endocrine adaptation, and translational implications.
PMID:日期:2026-09-14Cardiovascular disease is strongly influenced by mitochondrial dysfunction, yet how mitochondrial stress is communicated beyond the affected cell to coordinate systemic responses remains incompletely understood. Mitokines are stress-responsive signaling factors that link mitochondrial perturbation to cellular and interorgan adaptation. These include nuclear-encoded proteins such as fibroblast growth factor 21 (FGF21) and growth differentiation factor 15 (GDF15), as well as mitochondrial-derived peptides including Humanin and MOTS-c. This review critically examines mitokine regulation and signaling in the context of cardiovascular stress, with emphasis on mitochondrial unfolded protein response and integrated stress response pathways, receptor and downstream signaling mechanisms, and the functional divergence among major mitokines. Transient mitokine responses during physiological or metabolic challenge may support metabolic flexibility, cytoprotection, and stress adaptation, whereas persistent elevations of FGF21 and GDF15 in cardiovascular and cardiometabolic disease frequently accompany unresolved mitochondrial stress and adverse clinical phenotypes. Importantly, such associations do not establish that sustained mitokine signaling is itself maladaptive, and major mechanistic uncertainties remain, particularly for mitochondrial-derived peptides. We integrate these observations within a proposed "mitokine code" framework in which mitokine identity, relative patterns, temporal dynamics, and disease context may collectively provide information about mitochondrial stress and systemic adaptation. We further evaluate the potential and current limitations of mitokines as cardiovascular biomarkers and therapeutic targets. This framework positions mitokine signaling at the interface between mitochondrial dysfunction, systemic stress adaptation, and cardiovascular disease while identifying mechanistic and translational questions requiring prospective validation.
-
5. Neuroprotective effect of 3',4'-dihydroxyflavonol on blood-brain barrier ıntegrity and matrix remodeling in rats with transient bilateral carotid occlusion-ınduced ıschemia-reperfusion.
5. 3'，4'-二羟基黄酮醇对短暂性双侧颈动脉闭塞诱导的缺血再灌注大鼠血脑屏障完整性和基质重塑的神经保护作用PMID:日期:2026-09-05The reduced blood flow and energy substrates to the affected area during ischemia and sudden exposure to these molecules after ischemia is called reperfusion. Reperfusion can be as damaging to cells and tissues as ischemia. This study aims to examine the effects of brain Ischemia-Reperfusion (I/R) and 1-week 3',4'-Dihydroxyflavonol (DiOHF) treatment on Matrix Metalloproteinasease (MMP), occludin, claudin-5, and β-actin levels in frontal cortex and hippocampus tissue in male rats. In this study, twenty-eight male Wistar-Albino rats were allocated into four experimental groups: Control, Sham, Ischemia-Reperfusion (I/R), and Ischemia-Reperfusion + DiOHF. Under general anesthesia, bilateral carotid artery ligation was performed to induce ischemia for 30 min, followed by reperfusion. DiOHF supplementation (10 mg/kg) was administered for one week. At the end of the treatment period, the animals were sacrificed under general anesthesia, and the frontal cortex and hippocampus tissues were harvested. Gene expression levels of MMP-3, MMP-9, occludin, claudin-5, and β-actin in the collected tissues were analyzed using real-time PCR. While I/R suppressed the levels of claudin-5 and occludin in the frontal cortex and hippocampus, it increased the levels of β-actin, matrix metalloproteinase-3 (MMP-3), and matrix metalloproteinase-9 (MMP-9). 3',4'-Dihydroxyflavonol supplementation for 1 week corrected the deteriorations caused by I/R. The study results show that 1 week of 3',4'-Dihydroxyflavonol treatment after I/R corrects the changes in structural damage indicators caused by transient bilateral carotid occlusion-induced ischemia-reperfusion in the frontal cortex and hippocampus to a certain extent.
-
6. Protonophore uncouplers and the decoupler α,ω-hexadecanedioic acid relieve the succinate-induced blockade of glutamate and malate oxidation in the resting state (state 4).
6. 质子载体解偶联剂和解偶联剂α,ω-十六烷二酸在静息态（状态4）下缓解了琥珀酸引起的谷氨酸和苹果酸氧化的阻断PMID:日期:2026-08-26[中文摘要] 理论和实验研究表明，在缺乏ATP合成的肝脏线粒体中（状态4），琥珀酸与谷氨酸和苹果酸混合物的氧化，如同单独氧化琥珀酸一样，在质子动力势的生成中仅涉及复合体III和IV，而不泵送质子的复合体II则氧化琥珀酸。因此，琥珀酸氧化抑制谷氨酸和苹果酸的氧化，可能是通过在复合体I处诱导反向电子传递（RET）并抑制NADH氧化来实现的。观察到琥珀酸对谷氨酸和苹果酸氧化阻断作用的半最大效应浓度为220 ± 25 µM，这与生理条件下各种器官和组织细胞中的浓度相对应。质子载体解偶联剂n-三氟甲氧基羰基氰基苯腙（FCCP）、棕榈酸（PA）和鹅去氧胆酸（CDCA），在其刺激呼吸不超过两倍的条件下，可减轻琥珀酸对谷氨酸和苹果酸氧化的抑制。解偶联剂α,ω-十六烷二酸（HDA）在刺激线粒体呼吸1.5倍的条件下，同样可减轻琥珀酸对谷氨酸和苹果酸氧化的抑制作用。值得注意的是，与质子载体解偶联剂不同，HDA的这一效应可能与呼吸链复合体III切换至空转模式有关。在谷氨酸和苹果酸氧化过程中，即正向电子传递条件下，质子载体解偶联剂FCCP、PA和CDCA抑制肝脏线粒体H₂O₂的生成，而HDA无效。在琥珀酸及琥珀酸与谷氨酸和苹果酸混合物氧化过程中，即反向电子传递（RET）条件下，质子载体解偶联剂和HDA对肝脏线粒体H₂O₂生成的抑制作用程度大致相同。推测上述解偶联剂和HDA的这一效应可能与抑制RET有关，从而减轻琥珀酸对谷氨酸和苹果酸氧化的抑制作用。本研究表明，生理浓度的琥珀酸足以主导电子流，而经典解偶联剂和天然解偶联剂以及解偶联剂HDA均可逆转这一效应，尽管其机制途径不同。
[英文摘要] Theoretical and experimental studies have revealed that in liver mitochondria in the absence of ATP synthesis (state 4), the oxidation of a mixture of succinate with glutamate and malate, like the oxidation of succinate alone, involves only complexes III and IV in the generation of the proton motive force, while complex II, which does not pump protons, oxidizes succinate. Consequently, succinate oxidation suppresses the oxidation of glutamate and malate, likely by inducing reverse electron transport (RET) at complex I and inhibiting NADH oxidation. The concentration of succinate at which its half-maximal effect on blocking glutamate and malate oxidation is observed is 220 ± 25 µM, which corresponds to its concentration in cells of various organs and tissues under physiological conditions. The protonophore uncouplers n-trifluoromethoxycarbonylcyanide phenylhydrazone (FCCP), palmitic acid (PA), and chenodeoxycholic acid (CDCA), provided that they stimulate respiration no more than two-fold alleviate the suppression of glutamate and malate oxidation by succinate. The decoupler α,ω-hexadecanedioic acid (HDA), upon stimulating mitochondrial respiration by 1.5-fold, also alleviates the suppressive effect of succinate on glutamate and malate oxidation. It is noted that, unlike protonophore uncouplers, this effect of HDA may be associated with switching complex III of the respiratory chain to an idle mode of operation. During the oxidation of glutamate and malate, i.e., under conditions of forward electron transport, the protonophore uncouplers FCCP, PA, and CDCA inhibit HO generation by liver mitochondria, whereas HDA is ineffective. During the oxidation of succinate and the mixture of succinate with glutamate and malate, i.e., under conditions of reverse electron transport (RET), protonophore uncouplers and HDA inhibit HO generation by liver mitochondria to approximately the same extent. It is suggested that this effect of the aforementioned uncouplers and HDA is likely related to the inhibition of RET and, consequently, to the alleviation of the suppressive effect of succinate on glutamate and malate oxidation. This study demonstrates that the physiological concentration of succinate is sufficient to dominate electron flow, and that both classical and natural uncouplers, as well as the decoupler HDA, can reverse this effect, albeit via different mechanistic pathways.
-
7. M2 macrophage-derived exosomal EHF transcriptionally activates FGFR1 to promote malignant phenotypes and glycolysis in NSCLC.
7. M2巨噬细胞衍生的外泌体EHF转录激活FGFR1促进NSCLC的恶性表型和糖酵解PMID:日期:2026-08-11Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, largely due to the supportive role of the tumor microenvironment (TME). Tumor-associated macrophages, particularly the M2 phenotype, are pivotal in promoting NSCLC progression. Exosomes, key mediators of intercellular communication, can transfer functional cargo from M2 macrophages to cancer cells, thereby regulating malignant behaviors. However, the specific mechanisms by which M2 macrophage-derived exosomes modulate NSCLC progression are not fully understood. Bioinformatics analyses were initially performed to identify differentially expressed genes (DEGs) in M2 macrophages and NSCLC tissues using the GSE159112 and GSE268175 datasets. THP-1 cells were induced to differentiate into M2 macrophages, from which exosomes were isolated and characterized via nanoparticle tracking analysis, transmission electron microscopy, and western blotting. NSCLC cell lines (A549 and H23) were co-cultured with these exosomes to assess the transfer of ETS homologous factor (EHF). Functional assays, including 5-Ethynyl-2'-deoxyuridine (EdU), Transwell, flow cytometry, and sphere formation assays, were conducted to evaluate cell proliferation, migration, invasion, apoptosis, and stemness. Glycolytic capacity was determined by measuring glucose uptake, lactate production, and ATP levels. Chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays were employed to verify the transcriptional regulation of FGFR1 by EHF. Rescue experiments involving FGFR1 overexpression were performed to validate the signaling axis, and a xenograft mouse model was established to confirm the in vivo findings. EHF was identified as a critical upregulated transcription factor in both M2 macrophages and NSCLC tissues. M2 macrophage-derived exosomes were efficiently internalized by NSCLC cells, resulting in subsequent upregulation of its expression in recipient cells. Mechanistically, EHF transcriptionally activated fibroblast growth factor receptor 1 (FGFR1) by binding to its promoter region. Functionally, exosomes derived from EHF-deficient M2 macrophages significantly suppressed NSCLC cell proliferation, migration, invasion, and sphere formation, while promoting apoptosis. Concurrently, the loss of exosomal EHF inhibited glycolysis, evidenced by reduced glucose uptake, lactate production, and ATP levels. Crucially, restoring FGFR1 expression reversed the suppressive effects induced by EHF-deficient exosomes, confirming that the EHF/FGFR1 axis drives these malignant phenotypes. In vivo experiments further demonstrated that exosomes from EHF-silenced M2 macrophages inhibited tumor growth and downregulated proliferation markers. M2 macrophage-derived exosomal EHF promoted NSCLC progression and glycolysis by transcriptionally activating FGFR1. These findings highlight the EHF/FGFR1 axis as a novel molecular link between macrophages and NSCLC cells.
-
8. Fluoride exposure induces oxidative damage in primary astrocytes of SD rats and changes in the expression of α-synuclein and its effect on Nrf2-NQO1/HO-1 signaling pathway.
8. 氟暴露诱导 SD 大鼠原代星形胶质细胞氧化损伤及 α-突触核蛋白表达变化及其对 Nrf2-NQO1/HO-1 信号通路的影响PMID:日期:2026-08-07[中文摘要] 长期过量摄入氟化物会在脑组织中蓄积，引起神经元变性和神经系统功能障碍。其机制与氧化应激升高密切相关。α-突触核蛋白（α-Syn）表达于神经元突触前终末，在环境毒素暴露或氧化应激条件下，其表达发生变化并错误折叠为具有细胞毒性的寡聚体和聚集体，诱导氧化性细胞损伤。同时，核因子E2相关因子2（Nrf2）-NAD(P)H：醌氧化还原酶1（NQO1）/血红素加氧酶-1（HO-1）通路是调节氧化损伤的重要细胞系统，其核心激酶主要表达于脑星形胶质细胞。本研究旨在探讨氟暴露对星形胶质细胞氧化应激水平的影响以及Nrf2-NQO1/HO-1通路内α-Syn的表达。原代星形胶质细胞经细胞外α-突触核蛋白预成纤维（αSP）处理并联合氟暴露。结果表明，氟暴露诱导原代星形胶质细胞反应性活化，活性氧（ROS）水平升高，超氧化物歧化酶（SOD）和过氧化氢酶（CAT）活性降低，并上调Nrf2-NQO1/HO-1通路的蛋白表达。αSP引起原代星形胶质细胞氧化应激，并加剧氟暴露诱导的氧化损伤。这些发现对于加深理解慢性氟中毒相关脑损伤的机制具有重要意义。
[英文摘要] Long-term excessive fluoride intake accumulates in brain tissue, causing neuronal degeneration and nervous system dysfunction. This mechanism is closely related to elevated oxidative stress. α-Synuclein (α-Syn) is expressed in neuronal presynaptic terminals; under environmental toxin exposure or oxidative stress, its expression changes and it misfolds into oligomers and aggregates that are cytotoxic and induce oxidative cellular damage. Meanwhile, the nuclear factor erythroid 2-related factor 2 (Nrf2)-NAD(P)H: quinone oxidoreductase 1 (NQO1)/heme oxygenase-1 (HO-1) pathway is an important cellular system for regulating oxidative damage, and its core kinase is mainly expressed in brain astrocytes.The aim of this study is to investigate the effects of fluoride exposure on oxidative stress levels in astrocytes and the expression of α-Syn within the Nrf2-NQO1/HO-1 pathway. Primary astrocytes were treated with extracellular α-synuclein pre-formed fibrils (αSP) in conjunction with fluoride exposure. The results demonstrated that fluoride exposure induced reactive activation of primary astrocytes, increased levels of reactive oxygen species (ROS), decreased activities of superoxide dismutase (SOD) and catalase (CAT), and up-regulated the protein expression within the Nrf2-NQO1/HO-1 pathway. αSP caused oxidative stress in primary astrocytes and exacerbated oxidative damage induced by fluoride exposure. These findings are significant for enhancing the understanding of the mechanisms underlying brain injury associated with chronic fluorosis.
-
10. Par-4/TERT induced autophagy dysregulation in regulating glycolysis in hyperglycemia combined with hepatocellular carcinoma.
PMID:日期:2026-07-31To explore the mechanism by which the Prostate apoptosis response-4 (Par-4)/Telomerase Reverse Transcriptase (TERT) axis induces tumor progression by regulating autophagy and glycolysis in hepatocellular carcinoma (HCC) under hyperglycemic conditions. The high-glucose Hepa1-6 cell model and nude mouse HCC xenograft model were used, along with gene knockdown (shPar-4, shTERT) and overexpression (oePar-4) strategies. Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assay, flow cytometry, Western blot, TUNEL staining, co-immunoprecipitation (co-IP), quantitative real-time PCR (qPCR), and animal experiments were performed to analyze the effects of Par-4/TERT on AKT activity, autophagic activity, and the expression of key glycolytic enzymes (GLUT-1, HK, PFK, and PK). The anti-tumor effects of AKT inhibitors (SH-5 and LY294002), the autophagy regulator (rapamycin), and the glycolysis inhibitor (2-deoxy-D-glucose, 2-DG) were further evaluated. Under hyperglycemic conditions, Par-4 expression was significantly suppressed, whereas TERT expression was markedly upregulated. This elevated TERT expression activated the AKT/NF-κB/FOXO3a signaling pathway, leading to enhanced glycolytic metabolism (evidenced by upregulated expression of glucose transporters such as GLUT-1 and key glycolytic enzymes) and induced autophagic processes (characterized by increased LC3-II/LC3-I ratios and decreased p62 levels). Par-4 overexpression or TERT knockdown effectively reversed these effects, resulting in inhibited cell proliferation and induced apoptosis. Co-immunoprecipitation (co-IP) experiments confirmed a direct interaction between Par-4 and TERT, with Par-4 negatively regulating TERT expression. In combination therapeutic approaches, the LY294002 + 2-DG regimen exhibited synergistic anti-tumor efficacy in models with Par-4 overexpression or TERT knockdown, achieving a greater than 50% reduction in tumor volume accompanied by downregulated p62 expression. The Par-4/TERT regulatory axis modulates autophagy dysregulation and glycolytic metabolism through the AKT signaling cascade, contributing to HCC progression under hyperglycemic conditions. Synergistic targeting of this axis, in conjunction with AKT blockade and glycolytic inhibition, exerts potent anti-tumor activity, providing a novel precision therapeutic strategy for HCC associated with hyperglycemia.