Autophagy自噬
Autophagy(英文缩写 AUTOPHAGY),ISSN 1554-8627,eISSN 1554-8635,中文译名:自噬 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 | 13.391 | Q1 |
| 2022 | 13.300 | Q1 |
| 2023 | 14.600 | Q1 |
| 2024 | 14.300 | Q1 |
| 2025 | 18.600 | Q1 |
Autophagy 最新收录文献
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1. RABC1 regulates ER-phagy to maintain ER homeostasis in plants.
PMID:日期:2026-10-04Endoplasmic reticulum (ER)-phagy is an important ER quality-control pathway that selectively removes misfolded or unfolded proteins and damaged ER membranes through autophagic degradation in the vacuole. Recent studies have identified small guanosine triphosphatases (GTPases) as important regulators of the autophagy pathway. However, how they couple stress signals to ER-phagy remains poorly understood in plants. Our recent work demonstrated that RABC1 regulates ER-phagy under dithiothreitol (DTT)-, tunicamycin (TM)-, and heat-induced ER stress through interaction with the exocyst complex component SEC5A. Upon ER stress, green fluorescent protein (GFP)-RABC1 was recruited to the ATG8e-positive autophagosomes from the ER and Golgi in root cells, whereas autophagic flux and calnexin 1 (CNX1)-mRFP-tagged ER membranes turnover were impaired in the mutant. Together, our findings support a model in which RABC1 acts as a molecular switch that interacts with distinct effectors to regulate autophagy under different stress conditions. RAB, ras-related in brain; ER, endoplasmic reticulum; GTPases, guanosine triphosphatases; GFP, green fluorescent protein; CNX1, calnexin 1; GDP, guanosine diphosphate; GTP, guanosine triphosphate; SAR1D, secretion associated ras related GTPase 1D; COPII, coat protein complex II; LDs, lipid droplets; DTT, dithiothreitol; TM, tunicamycin; TOR, target of rapamycin; ATG, autophagy-related; Rho, ras homology.
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2. It's apples and oranges (or chalk and cheese, depending on where you live): RPM versus RCF.
PMID:日期:2026-09-25At we request that authors express centrifugal values as relative centrifugal force (RCF) or g-force as opposed to revolutions per minute (RPM). This is not an arbitrary decision but to understand the reason we need to provide a brief explanation of the difference between these two terms and, yes, there is a difference. Hence, it is annoying when during the editing process we request that an author convert a stated value such as "12,000 RPM" to "×g" and they simply return the paper with "12,000 ×g." The problem is that "12,000 RPM" is not equivalent to "12,000 ×g."
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3. Thyroid hormone promotes lipid droplet remodeling and lipophagy through KAT2B/PCAF-dependent histone acetylation in preimplantation embryos.
3. 甲状腺激素通过KAT2B/PCAF依赖的组蛋白乙酰化促进着床前胚胎中的脂滴重塑和脂噬PMID:日期:2026-09-24Thyroid hormones are central regulators of metabolic homeostasis and developmental programming. The active hormone triiodothyronine (T3) modulates transcription through nuclear receptors that recruit epigenetic cofactors to remodel chromatin and regulate metabolic gene networks. Although thyroid hormone signaling is known to influence lipid metabolism, whether it coordinates lipid droplet turnover with autophagy-related pathways during early embryonic development remains largely unknown. Here, transcriptomic profiling revealed distinct metabolic signatures between and embryos, with marked differences in fatty acid metabolism. Supplementation with 50 nM T3 enhanced blastocyst formation, particularly when applied from the 4-cell to blastocyst stages, coinciding with elevated thyroid hormone receptor expression. T3 induced robust lipid droplet remodeling, characterized by reduced droplet size, together with increased lipid-mitochondria colocalization and activation of lysosomal and mitochondrial pathways, consistent with enhanced lipid catabolism and organelle coupling. Mechanistically, inhibition of the histone acetyltransferase KAT2B/PCAF abolished T3-mediated developmental gains, reduced H3K9ac and H3K27ac, and resulted in nonselective autophagic stress rather than lipophagy. By contrast, T3 required KAT2B to stimulate cytosolic lipolysis, channel fatty acids into mitochondria, and enhance mitochondrial membrane potential. T3 also upregulated prostaglandin biosynthesis genes and improved outgrowth performance. These findings identify a thyroid hormone-KAT2B epigenetic axis that coordinates lipid droplet remodeling through lipolytic and lipophagic pathways, linking endocrine signaling to organelle crosstalk and mitochondrial activation during early embryogenesis. ART: assisted reproductive technology; ATG5: autophagy related 5; BSA: bovine serum albumin; BSCL2/SEIPIN: BSCL2 lipid droplet biogenesis associated, seipin; CARM1: coactivator associated arginine methyltransferase 1; COCs: cumulus-oocyte complexes; CPT1A: carnitine palmitoyltransferase 1A; CPT2: carnitine palmitoyltransferase 2; CREBBP/CBP: CREB binding protein; DEGs: differentially expressed genes; DGAT1: diacylglycerol O-acyltransferase 1; EP300: E1A binding protein p300; ER: endoplasmic reticulum; H3K9ac: histone H3 acetyl-Lys9; H3K27ac: histone H3 acetyl-Lys27; HCS: high-content screening; HDACs: histone deacetylases; IVC: in vitro culture; IVF: in vitro-fertilized embryos; IVM: in vitro maturation; IVO: in vivo embryos; KAT2A/GCN5: K(lysine) acetyltransferase 2A; KAT2B/PCAF: K(lysine) acetyltransferase 2B; KAT2Bi (Ki): KAT2B inhibition; KD: knockdown; LC3: microtubule associated protein 1 light chain 3; LDs: lipid droplets; LIPE/HSL: lipase E, hormone sensitive type; MGLL: monoglyceride lipase; MMP: mitochondrial membrane potential; mtDNA: mitochondrial DNA; MT-ND1: mitochondrially encoded NADH:ubiquinone oxidoreductase core subunit 1; PA: parthenogenetically activated; PG: prostaglandin; PLA2G4A: phospholipase A2 group IVA; PLIN2: perilipin 2; PLIN3: perilipin 3; PLIN5: perilipin 5; PNPLA2/ATGL: patatin like phospholipase domain containing 2; PPARD/PPARδ: peroxisome proliferator activated receptor delta; PPARs: peroxisome proliferator activated receptors; PRMT1: protein arginine methyltransferase 1; PTGS1: prostaglandin-endoperoxide synthase 1; PTGS2: prostaglandin-endoperoxide synthase 2; PVA: polyvinyl alcohol; RT: room temperature; RT-qPCR: reverse transcription-quantitative polymerase chain reaction; RXR: retinoid X receptor; SIRT1: sirtuin 1; SLC25A20/CACT: solute carrier family 25 member 20; SLC27A4/FATP4: solute carrier family 27 member 4; SUV39H1: SUV39H1 histone lysine methyltransferase; T3: triiodothyronine; T4: thyroxine; TAGs: triacylglycerols; TEM: transmission electron microscopy; THR: thyroid hormone receptor; THRA: thyroid hormone receptor alpha; THRA-i: thyroid hormone receptor antagonist; THRB: thyroid hormone receptor beta; THs: thyroid hormones; ZGA: zygotic genome activation.
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4. Methyl-HLH-30/TFEB orchestrates holistic intestinal recuperation against bacterial pore-forming toxin intoxication via TTC38 in metazoans.
PMID:日期:2026-09-23Effector-triggered immunity (ETI) safeguards intestinal epithelial cells (IECs) by surveilling bacterial virulence effectors or the damage they cause, such as pore-forming toxins (PFTs) that breach plasma membrane integrity (PMI). However, how metazoan ETI regulators guard IEC homeostasis compromised by PFT remains elusive. Moreover, while the molecular architectures of ETI are well-defined in plants, functionally analogous systems in animals are only beginning to emerge. Here, we unveil a conserved ETI guard system - the intestinal ETI regulator methyl-HLH-30/TFEB upregulates a novel intrinsic cellular defense (INCED) orchestrator Y54G11A.4/TTC38 - in and human IECs. This conserved ETI system coordinates the restoration of PMI, microvilli architecture, and nutrient absorption concurrently by promoting phase condensation of the PTRN-1/CAMSAP-dependent guard program through an HSPA/HSP70-HSP90 chaperone system. Together, our findings reveal an intestinal ETI guard system that couples PFT-damage sensing to comprehensive epithelial recuperation, underscoring its physiological relevance for mucosal homeostasis across metazoans. (Bt): ; CAMSAP: calmodulin regulated spectrin associated protein; : ; Cry toxins: crystal toxins; ETI: effector-triggered immunity; FRAP: fluorescence recovery after photobleaching; FRET: Förster/fluorescence resonance energy transfer; GFP: green fluorescent protein; /HLH: helix loop helix; HSP: heat shock protein; IDRs: intrinsically disordered regions; IECs: intestinal epithelial cells; INCED: intrinsic cellular defense; IPTG: isopropyl-β-D-1-thiogalactopyranoside; /LGG: LC3 and GABARAP family; ncMTOC: non-centrosomal microtubule-organizing center; LLPS: liquid-liquid phase separation; PFTs: pore-forming toxins; PI: propidium iodide; PMI: plasma membrane integrity; PTMs: post-translational modifications; qRT-PCR: quantitative real-time PCR; RNAi: ribonucleic acid interference; SEM: scanning electron microscopy; SLO: streptolysin O; SQST-1/SQSTM1/p62: sequestosome related 1; TFEB: transcription factor EB; TPR: tetratricopeptide repeat motifs; TTC38: tetratricopeptide repeat domain 38.
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5. CD81 drives immune evasion in radioresistant glioblastoma by blocking selective autophagic degradation of CD274/PD-L1.
5. CD81通过阻断CD274/PD-L1的选择性自噬降解驱动放射抵抗性胶质母细胞瘤的免疫逃逸PMID:日期:2026-09-22Glioblastoma multiforme (GBM) is the most aggressive primary brain tumor, for which radiotherapy constitutes the key component of standard comprehensive treatment; however, tumor relapse could inevitably arise from intrinsically radioresistant GBM subclones. Radiotherapy exerts biphasic regulatory effects on the tumor immune microenvironment (TIME), with transient activation followed by sustained immunosuppression. Nevertheless, it remains elusive how radioresistant GBM cells remodel such an immunosuppressive TIME to evade immune surveillance. Herein, integrative analyses encompassing clinical specimens, public single-cell RNA-seq datasets, orthotopic glioma models, primary CD8 T cell co-culture systems, and tandem mass tag (TMT) proteomics indicated that CD81 was highly expressed in radioresistant GBM and governed GBM immune evasion. CD81-high tumor cells were surrounded by functionally exhausted CD8 T cells, alongside immunosuppressive signature within neighboring myeloid and NK cells. CD81 depletion promoted selective macroautophagic/autophagic degradation of CD274/PD-L1, increased CD8 T cell infiltration and cytotoxic activity, reduced M2-like tumor-associated macrophages, and suppressed intracranial tumor growth. Moreover, CD81-knockdown augmented the antitumor efficacy of anti-PDCD1/PD-1, yielding a pronounced survival benefit when combined with radiotherapy. Mechanistically, CD81 interacted with CD274 via its large extracellular loop (LEL) and recruited the deubiquitinase USP14 through its cytoplasmic C-terminal tail (CCT). This resultant ternary complex erased K63-linked ubiquitination at the K280 residue of CD274, thereby abolishing SQSTM1/p62-dependent recognition and subsequent autophagy-lysosomal degradation of CD274 to maintain its protein stability. Collectively, our work establishes CD81 as a pivotal bridge connecting radioresistance to immune escape via sustaining CD274 abundance in GBM, highlighting CD81 as a promising therapeutic target to optimize radioimmunotherapy. BBB: blood-brain barrier; CTLs: cytotoxic T lymphocytes; CCK-8: cell counting kit-8; ELISA: enzyme-linked immunosorbent assay; GBM: glioblastoma; IHC: Immunohistochemistry; GZMB: granzyme B; MDSCs: myeloid-derived suppressor cells; MAP1LC3/LC3: microtubule associated protein 1 light chain 3; OS: overall survival; PFA: paraformaldehyde; PLA: proximity ligation assay; PRF1: Perforin1; STR: short tandem repeat; SQSTM1: sequestosome 1; TMT: tandem mass tag; TMZ: temozolomide; TME: tumor microenvironment; TDEs: tumor-derived exosomes; T: regulatory T cells; WT: wild type.
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6. Spatial control of mitochondrial ubiquitination by the AMBRA1-RMC1-HUWE1 axis.
PMID:日期:2026-09-20Mitochondrial ubiquitination is a central component of mitochondrial quality control. The PINK1 (PTEN induced kinase 1)-PRKN (parkin RBR E3 ubiquitin protein ligase) pathway established how loss of mitochondrial membrane potential can trigger a phospho-ubiquitin feed-forward cascade on the outer mitochondrial membrane (OMM). It remains less clear how mitochondrial ubiquitination is achieved when PRKN is absent or inactivated. In our recent work, we identify a recruitment platform organized by AMBRA1 (autophagy and beclin 1 regulator 1), in which RMC1 (regulator of MON1-CCZ1) positions HUWE1 (HECT, UBA and WWE domain containing E3 ubiquitin protein ligase 1) at mitochondria. This spatial arrangement promotes HUWE1-dependent ubiquitination and turnover of OMM proteins, including MFN2 (mitofusin 2), VDAC1 (voltage-dependent anion channel 1), and VDAC2 (voltage-dependent anion channel 2). Our findings raise the question of how cells select among distinct mitochondrial ubiquitination pathways and whether these pathways function independently, sequentially, or cooperatively.
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7. {"_":"Marked for destruction? When -nitrosylation writes protein fate through metabolic rewiring.","i":["S"]}
PMID:日期:2026-09-20Metabolism and autophagy are closely interconnected, but whether metabolic alterations can chemically modify proteins and influence their selective autophagic degradation remains poorly understood. Our recent findings show that increased -nitrosylation resulting from the loss of the denitrosylase AKR1A1/SCoR impairs glycolysis and promotes methylglyoxal accumulation, leading to carbonyl modification and selective autophagic degradation of KEAP1. These findings suggest that metabolic rewiring can influence the fate of specific proteins. In particular, we discuss whether glycation may act as a metabolic "mark" for selective autophagy and how the removal of metabolically modified proteins may, in turn, sustain signaling pathways involved in tumor progression and therapy resistance.
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8. Spatiotemporal control of Atg9 vesicle fusion in autophagosome formation.
PMID:日期:2026-09-16Atg9 vesicles serve as membrane seeds for autophagosome formation. These vesicles are derived from the Golgi/endosomes and localized to the pre-autophagosomal structure or phagophore assembly site (PAS) upon autophagy induction. How these vesicles are maintained as discrete membrane carriers while diffusing through the cytoplasm and subsequently become competent for downstream events at the PAS has remained unknown. Here, we show that the Atg9-interacting protein Atg23 remains associated with Atg9 vesicles following their formation and protects them from inappropriate fusion with endomembranes during their movement through the cytoplasm. Upon arrival at the PAS, Atg1-mediated phosphorylation of Atg9 triggers the dissociation of Atg23, thereby enabling efficient recruitment of the lipid-transfer protein Atg2. Collectively, these findings define a spatiotemporally regulated mechanism in which Atg23 preserves Atg9 vesicles during cytoplasmic transport, whereas its dissociation enables their productive utilization in autophagosome formation.
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9. Autophagic degradation of RAB8A promotes ferroptosis through dysregulation of TFRC-mediated iron uptake.
PMID:日期:2026-09-16Ferroptosis is an iron-dependent form of regulated cell death driven by lipid peroxidation; however, how selective autophagy regulates ferroptotic sensitivity remains incompletely understood. Here, we identify RAB8A as a selective autophagic substrate and negative regulator of ferroptosis. Quantitative proteomic analyses reveal that ferroptotic stress induces ATG5- and ATG7-dependent degradation of RAB8A. Mechanistically, ferroptotic stimuli induce RNF126-dependent polyubiquitination of RAB8A and subsequent SQSTM1-mediated autophagic degradation. Functionally, loss of sensitizes cancer cells to ferroptosis, whereas expression of the degradation-resistant active mutant RAB8A suppresses ferroptotic cell death. RAB8A interacts with TFRC and facilitates stress-induced redistribution of TFRC from the plasma membrane toward endolysosomal compartments. deficiency impairs TFRC clearance, enhances transferrin-dependent iron uptake, and increases intracellular Fe accumulation and lipid peroxidation. In fibrosarcoma and pancreatic cancer xenograft models, depletion enhances the antitumor efficacy of ferroptosis-inducing therapy. Clinically, RAB8A is upregulated and associated with poor prognosis and ferroptosis resistance in pancreatic cancer. Collectively, these findings establish an autophagy-RAB8A-TFRC axis that regulates ferroptotic sensitivity. BCA: bicinchoninic acid; BSA: bovine serum albumin; CCK-8: cellcounting kit-8; Co-IP: co-immunoprecipitation; DMSO: dimethylsulfoxide; ELISA: enzyme-linked immunosorbent assay; FBS: fetalbovine serum; HRP: horseradish peroxidase; IP: immunoprecipitation;LC-MS/MS: liquid chromatography-tandem mass spectrometry; MDA:malondialdehyde; MEF: mouse embryonic fibroblast; PBS:phosphate-buffered saline; PBS-T: PBS containing Tween-20; PI:propidium iodide; PVDF: polyvinylidene difluoride; qPCR: quantitativereal-time polymerase chain reaction; SDS: sodium dodecyl sulfate;STR: short tandem repeat; TBA: thiobarbituric acid; TBST:Tris-buffered saline containing Tween-20; TMT: tandem mass tag; WT:wild type.
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10. α-ketoglutarate ameliorates spinal motor neuron ferroptosis after sacral plexus transection via enhancing PINK1 O‑GlcNAcylation and mitophagy.
10. α-酮戊二酸通过增强PINK1 O-GlcNAc酰化修饰和线粒体自噬改善骶丛横断术后脊髓运动神经元铁死亡PMID:日期:2026-09-15Sacral plexus transection (SPT), mostly caused by high‑energy trauma, induces secondary death of spinal motor neurons in the lumbosacral segments and contributes to poor clinical outcomes after nerve repair. This study aimed to investigate the protective effect of α‑ketoglutarate (AKG) against ferroptosis in spinal motor neurons following SPT and the underlying molecular mechanism. Our results showed that endogenous AKG levels were significantly decreased in the spinal cord of SPT rats and in oxidative stress‑injured motor neurons, accompanied by abnormal expression of core ferroptosis‑related proteins, including downregulated glutathione peroxidase 4 and solute carrier family 7 member 11, upregulated acyl-CoA synthetase long-chain family member 4, as well as Fe overload, malondialdehyde accumulation, and glutathione depletion. Exogenous AKG supplementation markedly reversed these anomalies, suppressed ferroptosis, and improved neuronal survival. Mechanistically, AKG specifically enhanced O-GlcNAcylation at the Thr177 site of PTEN‑induced kinase 1 (PINK1) and suppressed its ubiquitin-mediated degradation, which in turn selectively activated PINK1-PRKN-dependent mitophagy to eliminate damaged mitochondria and sustain mitochondrial homeostasis. Furthermore, downregulation of isocitrate dehydrogenase 1 (IDH1) after SPT was identified as a critical upstream event leading to endogenous AKG depletion. This study systematically elucidates the key role of the IDH1‑AKG‑PINK1 O‑GlcNAcylation ‑mitophagy axis in regulating SPT‑induced ferroptosis in spinal motor neurons, providing novel targets and experimental evidence for neuroprotective therapy of sacral plexus injury.: ACSL4: acyl-CoA synthetase long-chain family member 4; AKG: 464748495051525354555657585960616263646566α‑ketoglutarate; BNIP3: BCL2/adenovirus E1B 19 kDa-interacting protein 3; CCK-8: cell counting kit-8; Co-IP: co-immunoprecipitation; Fer-1: ferrostatin-1; FUNDC1: FUN14 domain-containing 1; GLUD1: glutamate dehydrogenase 1; GPX4: glutathione peroxidase 4; GSH: glutathione; IDH1: isocitrate dehydrogenase 1; LC3: microtubuleassociated protein 1 light chain 3; MDA: malondialdehyde; MMP: mitochondrial membrane potential; NIX: NIP3-like protein X; O-GlcNAc: O-linked Nacetylglucosamine; OGT: O-GlcNAc transferase; OSMI-1: O-GlcNAc Transferase Inhibitor-1; PINK1: PTEN-induced kinase 1; PRKN: parkin RBR E3 ubiquitin protein ligase; ROS: reactive oxygen species; RT-qPCR: real-time quantitative polymerase chain reaction; siRNA: small interfering RNA; SLC7A11: solute carrier family 7 outer mitochondrial membrane 20.