Autophagy reports最新文献

BECLIN-1/BECN1 at the barrier: a gatekeeper of epithelial and endothelial homeostasis. 屏障中的BECLIN-1/BECN1：上皮和内皮稳态的看门人。

Autophagy reports Pub Date : 2025-10-05 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2566129

Juliani Juliani, Walter D Fairlie, Erinna F Lee

{"title":"BECLIN-1/BECN1 at the barrier: a gatekeeper of epithelial and endothelial homeostasis.","authors":"Juliani Juliani, Walter D Fairlie, Erinna F Lee","doi":"10.1080/27694127.2025.2566129","DOIUrl":"https://doi.org/10.1080/27694127.2025.2566129","url":null,"abstract":"Epithelial and endothelial barriers are essential for tissue homeostasis, protecting the body from environmental insults while regulating selective transport. The integrity of these barriers relies on dynamic intercellular junctions whose composition and organization are constantly remodeled in response to stress and physiological cues. Autophagy and endocytic trafficking are key intracellular pathways that maintain junctional stability and barrier resilience. BECLIN-1 (BECN1), a central regulator of both pathways, coordinates localized membrane dynamics through its interaction with the class III phosphatidylinositol 3-kinase (PtdIns3K) PIK3C3/VPS34. Recent advances reveal that BECN1's dual role in autophagy and endocytic trafficking is crucial for maintaining barriers in diverse tissues, including the gut, skin, and blood-brain barrier. Conversely, BECN1 dysfunction can compromise junctional integrity, driving inflammatory and degenerative diseases. This review summarizes the emerging evidence linking BECN1 to membrane trafficking, stress adaptation, and immune regulation across barrier tissues, highlighting its potential as a therapeutic target for barrier-associated diseases.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2566129"},"PeriodicalIF":0.0,"publicationDate":"2025-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12502826/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145254052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Revisiting the evolution of the yeast Atg1 complex. 回顾酵母Atg1复合体的进化。

Autophagy reports Pub Date : 2025-09-29 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2555835

Kha M Nguyen, Hannah R Shariati, Calvin K Yip

{"title":"Revisiting the evolution of the yeast Atg1 complex.","authors":"Kha M Nguyen, Hannah R Shariati, Calvin K Yip","doi":"10.1080/27694127.2025.2555835","DOIUrl":"10.1080/27694127.2025.2555835","url":null,"abstract":"The budding yeast Saccharomyces cerevisiae Atg1 complex coordinates the initiation of nonselective autophagy and consists of the Atg1 kinase, Atg13 regulatory subunit, and an S-shaped scaffold formed by Atg17, Atg29, and Atg31. In contrast, the fission yeast Schizosaccharomyces pombe Atg1 complex incorporates Atg101 instead of Atg29 and Atg31 and features a rod-shaped Atg17 scaffold. The timing of this divergence and its impact on the structural evolution of Atg17 remain unclear. Our systematic composition analysis revealed that Atg101 is found in the Atg1 complex of several budding yeast species, including two that contain both Atg29/Atg31 and Atg101. Structural modeling and negative stain EM analysis indicated that budding yeast species with Atg101 exhibit a rod-shaped Atg17. Additionally, we found that the Atg13 HORMA domain of S. pombe may possess a stabilizing cap, suggesting an alternative function for Atg101. Collectively, our findings delineate the potential evolutionary trajectories of the Atg1 complex in yeast. Abbreviations: ATG, autophagy-related; BLAST, basic local alignment search tool; C-Mad2, closed Mad2; EAT, Early Autophagy Targeting/Tethering; EM, electron microscopy; His-MBP, histidine-maltose binding protein; HORMA, Hop1, Rev7, and Mad2; IDR, intrinsically disordered region; O-Mad2, open Mad2; iTOL, Interactive Tree of Life; PAS, phagophore assembly site; PI3K, phosphatidylinositol 3-kinase; PMSF, phenylmethylsulfonyl fluoride; pTM, predicted template modeling; RMSD, root mean square deviation; TOR, target of rapamycin; TORC1, TOR complex 1.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2555835"},"PeriodicalIF":0.0,"publicationDate":"2025-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12482441/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145208521","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Liver-specific loss of Atg9a perturbs lipid metabolism and hepatocyte integrity. 肝脏特异性Atg9a缺失会扰乱脂质代谢和肝细胞完整性。

Autophagy reports Pub Date : 2025-09-02 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2551028

Elodie Mailler, Asmita Singh, Michal Jarnik, Yan Li, Lynne Holtzclaw, Victoria Hoffmann, Sohtaro Mine, Paulina Stallcup, Laleh Ordoubadinia, Carlos M Guardia

引用次数: 0

Autophagy and Bacterial infections. 自噬和细菌感染。

Autophagy reports Pub Date : 2025-09-01 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2542904

Ken Cadwell, Clara Abraham, Shai Bel, Santosh Chauhan, Jörn Coers, María I Colombo, Jacob R Davis, Daniel Hofius, Hang Thi Thu Nguyen, Michinaga Ogawa, Craig R Roy, Feng Shao, Sayaka Shizukuishi, Christina L Stallings, Magdalena Szczesna, Gergory Taylor, Teresa Lm Thurston, Robert Watson, Thomas Wileman, Yue Xu, Dario S Zamboni

{"title":"Autophagy and Bacterial infections.","authors":"Ken Cadwell, Clara Abraham, Shai Bel, Santosh Chauhan, Jörn Coers, María I Colombo, Jacob R Davis, Daniel Hofius, Hang Thi Thu Nguyen, Michinaga Ogawa, Craig R Roy, Feng Shao, Sayaka Shizukuishi, Christina L Stallings, Magdalena Szczesna, Gergory Taylor, Teresa Lm Thurston, Robert Watson, Thomas Wileman, Yue Xu, Dario S Zamboni","doi":"10.1080/27694127.2025.2542904","DOIUrl":"10.1080/27694127.2025.2542904","url":null,"abstract":"Autophagy is an evolutionarily conserved cellular process that is prominent during bacterial infections. In this review article, we discuss how direct pathogen clearance via xenophagy and regulation of inflammatory products represent dual functions of autophagy that coordinate an effective antimicrobial response. We detail the molecular mechanisms of xenophagy, including signals that indicate the presence of an intracellular pathogen and autophagy receptor-mediated cargo targeting, while highlighting pathogen counterstrategies, such as bacterial effector proteins that inhibit autophagy initiation or exploit autophagic membranes for replication. Pathways that are related to autophagy, including LC3-associated phagocytosis (LAP) and conjugation of ATG8 to single membranes (CASM), are expanding the role of autophagy in antimicrobial defense beyond traditional double-membrane autophagosomes. Examination of Crohn disease-associated genes links impaired autophagy to inflammation and defective bacterial handling. We propose emerging concepts, such as effector-triggered immunity, where autophagy inhibition by pathogens triggers inflammatory defenses and discusses the therapeutic potential of modulating autophagy in infectious and inflammatory diseases.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2542904"},"PeriodicalIF":0.0,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12407897/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145002004","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Chaperone-mediated autophagy dysfunction in imiquimod-induced psoriasiform dermatitis. 伴蛋白介导的自噬功能障碍在吡喹莫德诱导的银屑病样皮炎。

Autophagy reports Pub Date : 2025-08-25 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2544061

Wei Zhao, Kainan Liao, Wei Song, Jing Wang, Chunlin Cai, Fusheng Zhou, Dandan Zang, Deping Xu, Haisheng Zhou

{"title":"Chaperone-mediated autophagy dysfunction in imiquimod-induced psoriasiform dermatitis.","authors":"Wei Zhao, Kainan Liao, Wei Song, Jing Wang, Chunlin Cai, Fusheng Zhou, Dandan Zang, Deping Xu, Haisheng Zhou","doi":"10.1080/27694127.2025.2544061","DOIUrl":"10.1080/27694127.2025.2544061","url":null,"abstract":"Psoriasis is a chronic inflammatory skin disease characterized by abnormal differentiation and hyperproliferation of epidermal keratinocytes. Autophagy plays a critical role in regulating the functions of immune cells, endothelial cells, and especially keratinocytes, contributing to the pathogenesis of psoriasis. However, the role of chaperone-mediated autophagy (CMA) in psoriatic keratinocytes has not been fully explored. Our study, for the first time, revealed that defective CMA is present in imiquimod (IMQ)-induced psoriasiform lesions. Importantly, activation of CMA significantly attenuated IMQ-induced phenotypes both in vitro and in vivo, including reduced skin lesion severity, decreased keratinocyte proliferation and differentiation, and lower cytokine secretion. Mechanistically, toll-like receptor 7 (TLR7), containing a specific KFERQ-like motif, is a substrate for CMA-mediated degradation. This process modulates IMQ-TLR7 signal activation in keratinocytes. CMA deficiency in psoriasis leads to increased TLR7 levels, which, in turn, enhances TLR7-NF-κB signaling pathway activation, ultimately contributing to dysregulated keratinocyte proliferation, differentiation, and cytokine secretion. This study provides novel evidence that defective CMA is present in IMQ-induced psoriasiform lesions and that CMA activation can attenuate IMQ-induced phenotypes by modulating TLR7 signaling in keratinocytes. These findings highlight the potential of CMA as a therapeutic target for psoriasis.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2544061"},"PeriodicalIF":0.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12380211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144980702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Sequestering sequestosome 1 via S-acylation in autophagy, Huntington disease, and beyond. 在自噬、亨廷顿病及其他疾病中通过s -酰化隔离封存体1。

Autophagy reports Pub Date : 2025-08-25 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2547975

Y Alshehabi, F Abrar, D D O Martin

{"title":"Sequestering sequestosome 1 via S-acylation in autophagy, Huntington disease, and beyond.","authors":"Y Alshehabi, F Abrar, D D O Martin","doi":"10.1080/27694127.2025.2547975","DOIUrl":"10.1080/27694127.2025.2547975","url":null,"abstract":"Protein mislocalization and aggregation are hallmark features in neurodegeneration. As proteins mislocalize, proteostasis deficiency and protein aggregation typically follow. Autophagy is a crucial pathway for the removal of protein aggregates to maintain neuronal health, but is impaired in various neurodegenerative diseases, including Huntington disease (HD). We identified S-acylation, a reversible lipid modification of proteins, as an important regulator in protein trafficking and autophagy. SQSTM1 (sequestosome 1/p62) is an essential selective autophagy receptor for the sequestration of ubiquitinated cargoes within autophagosomes and subsequent delivery into lysosomes for degradation. Recently, we reported that S-acylation of SQSTM1 at the di-cysteine motif C289,290 directs SQSTM1 to lysosomes. We further showed that SQSTM1 S-acylation is significantly reduced in brains from both HD patients and mouse HD model, which may result in the cargo sequestration defect within autophagosomes in HD. Treatment with palmostatin B, a deacylation inhibitor, significantly increases SQSTM1 localization to lysosomes. Our work highlights SQSTM1 S-acylation as a novel potential therapeutic strategy in HD. As a crucial autophagy component, our work suggests S-acylation of SQSTM1 may have a broader role in neurodegeneration.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2547975"},"PeriodicalIF":0.0,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12380206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144980729","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

During Aspergillus nidulans nitrogen-limited biofilm formation, mitophagy is independent of mitochondrial fission. 在中性曲霉氮限制生物膜形成过程中，线粒体自噬独立于线粒体裂变。

Autophagy reports Pub Date : 2025-08-22 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2547194

Hari Krishnan Balasubramanian, Stephen A Osmani

{"title":"During Aspergillus nidulans nitrogen-limited biofilm formation, mitophagy is independent of mitochondrial fission.","authors":"Hari Krishnan Balasubramanian, Stephen A Osmani","doi":"10.1080/27694127.2025.2547194","DOIUrl":"10.1080/27694127.2025.2547194","url":null,"abstract":"During chronic infections, biofilms are resistant to both antimicrobial agents as well as the host immune system, often giving rise to recalcitrant persister cells with reduced mitochondrial function rendering biofilm infections difficult to cure. How mitochondrial dynamics and fate are regulated during fungal biofilm formation is poorly understood. In this study, we used live cell microscopy to track mitochondrial morphology during Aspergillus nidulans in vitro biofilm formation. We show that mitochondria undergo fragmentation during early biofilm development, and that externally induced oxidative stress similarly induces mitochondrial fragmentation, indicating a role for redox regulation in this process. Deletion of core components of the mitochondrial fission machinery resulted in a swollen mitochondrial phenotype. Mitochondria in the fission-mutant strains are known not to complete fragmentation in response to externally induced oxidative stress, and we show that this results in a \"beads on a string\" phenotype. We further show that mitochondria remain unfragmented during biofilm formation in the fission-mutant strains, although other biofilm cellular modifications, like disassembly of microtubules, are unaffected. We report that mitophagy is triggered during biofilm development in nitrogen-limiting conditions independently of mitochondrial fission. This indicates mitochondrial fission is dispensable for mitophagy during biofilm development with limiting nitrogen. We further note that general autophagy, but notably not mitophagy, is triggered during biofilm development in carbon-limiting conditions, demonstrating differential regulation of mitochondrial fate in response to specific nutritional limitations during fungal biofilm formation.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2547194"},"PeriodicalIF":0.0,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12377116/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144980664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cell type-specific autophagy in human leukocytes: signatures of aging, sex, and nutrient restriction. 人类白细胞中细胞类型特异性自噬：衰老、性别和营养限制的特征。

Autophagy reports Pub Date : 2025-08-17 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2543560

Linh Vp Dang, Timothy J Sargeant

{"title":"Cell type-specific autophagy in human leukocytes: signatures of aging, sex, and nutrient restriction.","authors":"Linh Vp Dang, Timothy J Sargeant","doi":"10.1080/27694127.2025.2543560","DOIUrl":"10.1080/27694127.2025.2543560","url":null,"abstract":"Macroautophagy (referred to here as autophagy) is thought to play a critical role in aging and age-related disease, making it a priority for development of targeted human therapies. We developed a flow cytometry-based method to measure autophagic flux in 19 subpopulations from whole blood, using chloroquine (CQ) to inhibit lysosomal degradation, and the autophagy protein MAP1LC3B (microtubule associated protein 1 light chain 3 beta) isoform II/LC3B-II to measure autophagic flux (the acquisition and degradation of autophagic cargo over time). Autophagic flux varies by cell type and is higher in whole blood compared with RPMI culture media. Basal autophagic flux shows sex- and age-specific variations. Further, monocytes, but not T cells, respond robustly to amino acid starvation by increasing autophagy, with older individuals exhibiting stronger responses, particularly in non-classical monocytes. These findings underscore the importance of cell type-specific autophagy measurements to understand the effects of aging, sex and nutrition, to develop targeted interventions for age-related diseases.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2543560"},"PeriodicalIF":0.0,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12366816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144980727","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Biarylacetamides: a novel class of late-stage autophagy inhibitors. 双芳基乙酰酰胺：一类新的晚期自噬抑制剂。

Autophagy reports Pub Date : 2025-08-07 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2541597

Mélissa Lallier, Rani Robeyns, Freke Mertens, Angela Sisto, Guido R Y De Meyer, Koen Augustyns, Maya Berg, Winnok H De Vos, Vincent Timmerman, George M C Janssen, Peter van Veelen, Alexander L N van Nuijs, Nikolai Engedal, Wim Martinet, Pieter Van der Veken

{"title":"Biarylacetamides: a novel class of late-stage autophagy inhibitors.","authors":"Mélissa Lallier, Rani Robeyns, Freke Mertens, Angela Sisto, Guido R Y De Meyer, Koen Augustyns, Maya Berg, Winnok H De Vos, Vincent Timmerman, George M C Janssen, Peter van Veelen, Alexander L N van Nuijs, Nikolai Engedal, Wim Martinet, Pieter Van der Veken","doi":"10.1080/27694127.2025.2541597","DOIUrl":"10.1080/27694127.2025.2541597","url":null,"abstract":"Targeting autophagy is believed to hold great promise for the treatment of various diseases, including cancer. However, since the therapeutic efficacy of currently available autophagy-modulating drugs is limited by off-target effects and the requirement of high dosage, there is an urgent need to develop novel autophagy-targeting compounds. In this study, we report molecules of the biarylacetamide class as novel autophagy inhibitors. These molecules were identified via phenotypic high-throughput screening, and a series of analogues was subsequently synthesized. Among these, 5d and 5j were retained as potent autophagy blockers in HeLa and LNCaP cells. Both compounds inhibited autophagy at a late-stage in the pathway, as evidenced by the strong accumulation of RFP-GFP-LC3 puncta as well as LC3-II, GABARAP-II and SQSTM1 protein levels, resembling the effects obtained with the well-known late-stage autophagy inhibitor Bafilomycin A1. Quantitative proteome profiling combined with metabolomic and lipidomic studies revealed that 5j significantly altered lipid metabolism. These alterations included activation of the cholesterol biosynthesis pathway and changes in the distribution of key lipid classes, such as phospholipids, ceramides and triglycerides. Further mechanistic studies indicated that 5d and 5j triggered an ER stress response and may impair lysosomal function, as suggested by the accumulation of pro-cathepsin D. Collectively, these findings demonstrate that 5j is a novel and potent late-stage autophagy inhibitor with a distinct mechanism of action compared to currently available inhibitors.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2541597"},"PeriodicalIF":0.0,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12439681/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145082653","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The role of autophagy in the pathogenesis and treatment of multiple sclerosis. 自噬在多发性硬化发病机制和治疗中的作用。

Autophagy reports Pub Date : 2025-07-22 eCollection Date: 2025-01-01 DOI: 10.1080/27694127.2025.2529196

Giulio Righes, Luana Semenzato, Konstantinos Koutsikos, Veronica Zanato, Paolo Pinton, Carlotta Giorgi, Simone Patergnani

{"title":"The role of autophagy in the pathogenesis and treatment of multiple sclerosis.","authors":"Giulio Righes, Luana Semenzato, Konstantinos Koutsikos, Veronica Zanato, Paolo Pinton, Carlotta Giorgi, Simone Patergnani","doi":"10.1080/27694127.2025.2529196","DOIUrl":"10.1080/27694127.2025.2529196","url":null,"abstract":"Autophagy is a crucial cellular process responsible for the degradation and recycling of damaged or unnecessary components, maintaining cellular homeostasis and protecting against stress. Dysregulation of autophagy has been implicated in a variety of neurodegenerative diseases, including multiple sclerosis, Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, and Huntington's disease. Various types of autophagy exist, each with distinct mechanisms, such as macroautophagy, mitophagy, lipophagy, and chaperone-mediated autophagy. These processes are essential for the removal of toxic substrates like protein aggregates and dysfunctional mitochondria, which are vital for neuronal health. In neurodegenerative diseases, the impairment of these clearance mechanisms leads to the accumulation of harmful substances, which accelerate disease progression. Modulating autophagy has emerged as a promising therapeutic strategy, with ongoing studies investigating molecules that can either stimulate or regulate this process. However, despite its potential, significant challenges remain in translating preclinical findings into clinically effective treatments. In this review, we will explore the different types of autophagy, their roles in neurodegenerative diseases, and the therapeutic potential associated with modulating these processes.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"4 1","pages":"2529196"},"PeriodicalIF":0.0,"publicationDate":"2025-07-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296075/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144735825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0