Autophagy reports最新文献_第8页

Interplay between septins and ubiquitin-mediated xenophagy during Shigella entrapment. 志贺氏菌包埋过程中sepins与泛素介导的异种吞噬之间的相互作用。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-05-17 DOI: 10.1080/27694127.2023.2213541

Damián Lobato-Márquez, José Javier Conesa, Ana Teresa López-Jiménez, Michael E Divine, Jonathan N Pruneda, Serge Mostowy

{"title":"Interplay between septins and ubiquitin-mediated xenophagy during Shigella entrapment.","authors":"Damián Lobato-Márquez, José Javier Conesa, Ana Teresa López-Jiménez, Michael E Divine, Jonathan N Pruneda, Serge Mostowy","doi":"10.1080/27694127.2023.2213541","DOIUrl":"10.1080/27694127.2023.2213541","url":null,"abstract":"Septins are cytoskeletal proteins implicated in numerous cellular processes including cytokinesis and morphogenesis. In the case of infection by Shigella flexneri, septins assemble into cage-like structures that entrap cytosolic bacteria targeted by autophagy. The interplay between septin cage entrapment and bacterial autophagy is poorly understood. We used a correlative light and cryo-soft X-ray tomography (cryo-SXT) pipeline to study septin cage entrapment of Shigella in its near-native state. Septin cages could be identified as X-ray dense structures, indicating they contain host cell proteins and lipids consistent with their autophagy links. Airyscan confocal microscopy of Shigella-septin cages showed that septins and lysine 63 (K63)-linked ubiquitin chains are present in separate bacterial microdomains, suggesting they are recruited separately. Finally, Cryo-SXT and live-cell imaging revealed an interaction between septins and microtubule-associated protein light chain 3B (LC3B)-positive membranes during autophagy of Shigella. Collectively our data present a new model for how septin-caged Shigella are targeted to autophagy.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10264059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9671939","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

AUTOPHAGY IN THE EYE: FROM PHYSIOLOGY TO PATHOPHYSOLOGY. 眼睛中的自噬：从生理学到病理生理学。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-03-01 DOI: 10.1080/27694127.2023.2178996

Paloma B Liton, Kathleen Boesze-Battaglia, Michael E Boulton, Patricia Boya, Thomas A Ferguson, Ian G Ganley, Anu Kauppinnen, Gordon W Laurie, Noboru Mizushima, Hideaki Morishita, Rossella Russo, Jaya Sadda, Rajalekshmy Shyam, Debasish Sinha, Debra A Thompson, David N Zacks

{"title":"AUTOPHAGY IN THE EYE: FROM PHYSIOLOGY TO PATHOPHYSOLOGY.","authors":"Paloma B Liton, Kathleen Boesze-Battaglia, Michael E Boulton, Patricia Boya, Thomas A Ferguson, Ian G Ganley, Anu Kauppinnen, Gordon W Laurie, Noboru Mizushima, Hideaki Morishita, Rossella Russo, Jaya Sadda, Rajalekshmy Shyam, Debasish Sinha, Debra A Thompson, David N Zacks","doi":"10.1080/27694127.2023.2178996","DOIUrl":"10.1080/27694127.2023.2178996","url":null,"abstract":"Autophagy is a catabolic self-degradative pathway that promotes the degradation and recycling of intracellular material through the lysosomal compartment. Although first believed to function in conditions of nutritional stress, autophagy is emerging as a critical cellular pathway, involved in a variety of physiological and pathophysiological processes. Autophagy dysregulation is associated with an increasing number of diseases, including ocular diseases. On one hand, mutations in autophagy-related genes have been linked to cataracts, glaucoma, and corneal dystrophy; on the other hand, alterations in autophagy and lysosomal pathways are a common finding in essentially all diseases of the eye. Moreover, LC3-associated phagocytosis, a form of non-canonical autophagy, is critical in promoting visual cycle function. This review collects the latest understanding of autophagy in the context of the eye. We will review and discuss the respective roles of autophagy in the physiology and/or pathophysiology of each of the ocular tissues, its diurnal/circadian variation, as well as its involvement in diseases of the eye.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10078619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9708880","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

Protein disorder in the regulatory control of mitophagy. 有丝分裂调节控制中的蛋白质紊乱。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-08-01 DOI: 10.1080/27694127.2023.2242054

Sheridan Mikhail, Scott A Soleimanpour

{"title":"Protein disorder in the regulatory control of mitophagy.","authors":"Sheridan Mikhail, Scott A Soleimanpour","doi":"10.1080/27694127.2023.2242054","DOIUrl":"10.1080/27694127.2023.2242054","url":null,"abstract":"Mitophagy is a central component of the mitochondrial quality control machinery, which is necessary for cellular viability and bioenergetics. The E3 ubiquitin ligase CLEC16A (C-type lectin domain containing 16A) forms a tripartite mitophagy regulatory complex together with the E3 ligase RNF41 (ring finger protein 41) and the ubiquitin-specific peptidase USP8 (ubiquitin specific peptidase 8), yet CLEC16A structural/functional domains relevant for mitophagy are unknown. We identify that CLEC16A contains an internal intrinsically disordered region (IDR), which is important for CLEC16A function and stability. IDRs are flexible domains lacking fixed secondary structure and regulate an emerging number of diverse processes, yet they have been largely unstudied in mitophagy. We observe that the internal CLEC16A IDR is essential for CLEC16A degradation and is bound by RNF41 to promote CLEC16A turnover. This IDR also promotes assembly of the CLEC16A-RNF41-USP8 mitophagy regulatory complex. Thus, our study revealed the importance of IDRs in mitophagy via the regulation of CLEC16A abundance by RNF41, opening new structural insights into mitochondrial quality control.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10399515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10316274","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

Transcriptional pausing factor M1BP regulates cellular homeostasis by suppressing autophagy and apoptosis in Drosophila eye. 转录暂停因子M1BP通过抑制果蝇眼睛的自噬和细胞凋亡来调节细胞稳态。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-09-05 DOI: 10.1080/27694127.2023.2252307

Anuradha Venkatakrishnan Chimata, Hannah Darnell, Akanksha Raj, Madhuri Kango-Singh, Amit Singh

{"title":"Transcriptional pausing factor M1BP regulates cellular homeostasis by suppressing autophagy and apoptosis in Drosophila eye.","authors":"Anuradha Venkatakrishnan Chimata, Hannah Darnell, Akanksha Raj, Madhuri Kango-Singh, Amit Singh","doi":"10.1080/27694127.2023.2252307","DOIUrl":"10.1080/27694127.2023.2252307","url":null,"abstract":"During organogenesis cellular homeostasis plays a crucial role in patterning and growth. The role of promoter proximal pausing of RNA polymerase II, which regulates transcription of several developmental genes by GAGA factor or Motif 1 Binding Protein (M1BP), has not been fully understood in cellular homeostasis. Earlier, we reported that M1BP, a functional homolog of ZKSCAN3, regulates wingless and caspase-dependent cell death (apoptosis) in the Drosophila eye. Further, blocking apoptosis does not fully rescue the M1BPRNAi phenotype of reduced eye. Therefore, we looked for other possible mechanism(s). In a forward genetic screen, members of the Jun-amino-terminal-(NH2)-Kinase (JNK) pathway were identified. Downregulation of M1BP ectopically induces JNK, a pro-death pathway known to activate both apoptosis and caspase-independent (autophagy) cell death. Activation of JNK pathway components can enhance M1BPRNAi phenotype and vice-versa. Downregulation of M1BP ectopically induced JNK signaling, which leads to apoptosis and autophagy. Apoptosis and autophagy are regulated independently by their genetic circuitry. Here, we found that blocking either apoptosis or autophagy alone rescues the reduced eye phenotype of M1BP downregulation; whereas, blocking both apoptosis and autophagy together significantly rescues the M1BP reduced eye phenotype to near wild-type in nearly 85% progeny. This data suggests that the cellular homeostasis response demonstrated by two independent cell death mechanisms, apoptosis and autophagy, can be regulated by a common transcriptional pausing mechanism orchestrated by M1BP. Since these fundamental processes are conserved in higher organisms, this novel functional link between M1BP and regulation of both apoptosis and autophagy can be extrapolated to humans.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10512699/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41124334","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

Neurodegenerative disease-associated inclusion bodies are cleared by selective autophagy in budding yeast. 神经退行性疾病相关的包涵体在芽殖酵母中通过选择性自噬清除。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-08-07 DOI: 10.1080/27694127.2023.2236407

Austin Folger, Chuan Chen, Marie-Helene Kabbaj, Karina Frey, Yanchang Wang

{"title":"Neurodegenerative disease-associated inclusion bodies are cleared by selective autophagy in budding yeast.","authors":"Austin Folger, Chuan Chen, Marie-Helene Kabbaj, Karina Frey, Yanchang Wang","doi":"10.1080/27694127.2023.2236407","DOIUrl":"10.1080/27694127.2023.2236407","url":null,"abstract":"Protein misfolding, aggregation, and accumulation cause neurodegenerative disorders. One such disorder, Huntington's disease, is caused by an increased number of glutamine-encoding trinucleotide repeats CAG in the first exon of the huntingtin (HTT) gene. Mutant proteins of Htt exon 1 with polyglutamine expansion are prone to aggregation and form pathological inclusion bodies in neurons. Extensive studies have shown that misfolded proteins are cleared by the ubiquitin-proteasome system or autophagy to alleviate their cytotoxicity. Misfolded proteins can form small soluble aggregates or large insoluble inclusion bodies. Previous works have elucidated the role of autophagy in the clearance of misfolded protein aggregates, but autophagic clearance of inclusion bodies remains poorly characterized. Here we use mutant Htt exon 1 with 103 polyglutamine (Htt103QP) as a model substrate to study the autophagic clearance of inclusion bodies in budding yeast. We found that the core autophagy-related proteins were required for Htt103QP inclusion body autophagy. Moreover, our evidence indicates that the autophagy of Htt103QP inclusion bodies is selective. Interestingly, Cue5/Tollip, a known autophagy receptor for aggrephagy, is dispensable for this inclusion body autophagy. From the known selective autophagy receptors in budding yeast, we identified three that are essential for inclusion body autophagy. Amyloid beta peptide (Aβ42) is a major component of amyloid plaques found in Alzheimer's disease brains. Interestingly, a similar selective autophagy pathway contributes to the clearance of Aβ42 inclusion bodies in budding yeast. Therefore, our results reveal a novel autophagic pathway specific for inclusion bodies associated with neurodegenerative diseases, which we have termed IBophagy.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10482306/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10577732","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

Orchestration of autophagosome fusion by STRIPAK complex components in muscle tissue. 肌肉组织中STRIPAK复合成分对自噬体融合的协调作用。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-09-27 DOI: 10.1080/27694127.2023.2260670

Yungui Guo, Erika R Geisbrecht

引用次数: 0

Autophagy in protists and their hosts: When, how and why? 原生生物及其宿主的自噬：何时、如何以及为何？

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-03-09 DOI: 10.1080/27694127.2022.2149211

Patricia Silvia Romano, Takahiko Akematsu, Sébastien Besteiro, Annina Bindschedler, Vern B Carruthers, Zeinab Chahine, Isabelle Coppens, Albert Descoteaux, Thabata Lopes Alberto Duque, Cynthia Y He, Volker Heussler, Karine G Le Roch, Feng-Jun Li, Juliana Perrone Bezerra de Menezes, Rubem Figueiredo Sadok Menna-Barreto, Jeremy C Mottram, Jacqueline Schmuckli-Maurer, Boris Turk, Patricia Sampaio Tavares Veras, Betiana Nebai Salassa, María Cristina Vanrell

{"title":"Autophagy in protists and their hosts: When, how and why?","authors":"Patricia Silvia Romano, Takahiko Akematsu, Sébastien Besteiro, Annina Bindschedler, Vern B Carruthers, Zeinab Chahine, Isabelle Coppens, Albert Descoteaux, Thabata Lopes Alberto Duque, Cynthia Y He, Volker Heussler, Karine G Le Roch, Feng-Jun Li, Juliana Perrone Bezerra de Menezes, Rubem Figueiredo Sadok Menna-Barreto, Jeremy C Mottram, Jacqueline Schmuckli-Maurer, Boris Turk, Patricia Sampaio Tavares Veras, Betiana Nebai Salassa, María Cristina Vanrell","doi":"10.1080/27694127.2022.2149211","DOIUrl":"10.1080/27694127.2022.2149211","url":null,"abstract":"Pathogenic protists are a group of organisms responsible for causing a variety of human diseases including malaria, sleeping sickness, Chagas disease, leishmaniasis, and toxoplasmosis, among others. These diseases, which affect more than one billion people globally, mainly the poorest populations, are characterized by severe chronic stages and the lack of effective antiparasitic treatment. Parasitic protists display complex life-cycles and go through different cellular transformations in order to adapt to the different hosts they live in. Autophagy, a highly conserved cellular degradation process, has emerged as a key mechanism required for these differentiation processes, as well as other functions that are crucial to parasite fitness. In contrast to yeasts and mammals, protist autophagy is characterized by a modest number of conserved autophagy-related proteins (ATGs) that, even though, can drive the autophagosome formation and degradation. In addition, during their intracellular cycle, the interaction of these pathogens with the host autophagy system plays a crucial role resulting in a beneficial or harmful effect that is important for the outcome of the infection. In this review, we summarize the current state of knowledge on autophagy and other related mechanisms in pathogenic protists and their hosts. We sought to emphasize when, how, and why this process takes place, and the effects it may have on the parasitic cycle. A better understanding of the significance of autophagy for the protist life-cycle will potentially be helpful to design novel anti-parasitic strategies.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10104450/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9324014","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

Kinetics of autophagic activity in nanoparticle-exposed lung adenocarcinoma (A549) cells. 暴露于纳米粒子的肺腺癌（A549）细胞自噬活性动力学。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-03-15 DOI: 10.1080/27694127.2023.2186568

Arnold Sipos, Kwang-Jin Kim, Constantinos Sioutas, Edward D Crandall

{"title":"Kinetics of autophagic activity in nanoparticle-exposed lung adenocarcinoma (A549) cells.","authors":"Arnold Sipos, Kwang-Jin Kim, Constantinos Sioutas, Edward D Crandall","doi":"10.1080/27694127.2023.2186568","DOIUrl":"10.1080/27694127.2023.2186568","url":null,"abstract":"Autophagy, a homeostatic mechanism, is crucial in maintaining normal cellular function. Although dysregulation of autophagic processes is recognized in certain diseases, it is unknown how maintenance of cellular homeostasis might be affected by the kinetics of autophagic activity in response to various stimuli. In this study, we assessed those kinetics in lung adenocarcinoma (A549) cells in response to exposure to nanoparticles (NP) and/or Rapamycin. Since NP are known to induce autophagy, we wished to determine if this phenomenon could be a driver of the harmful effects seen in lung tissues exposed to air pollution. A549 cells were loaded with a fluorescent marker (DAPRed) that labels autophagosomes and autolysosomes. Autophagic activity was assessed based on the fluorescence intensity of DAPRed measured over the entire cell volume of live single cells using confocal laser scanning microscopy (CLSM). Autophagic activity over time was determined during exposure of A549 cells to single agents (50 nM Rapamycin; 80 μg/mL, 20 nm carboxylated polystyrene NP (PNP); or, 1 μg/mL ambient ultrafine particles (UFP) (<180 nm)), or double agents (Rapamycin + PNP or Rapamycin + UFP; concomitant and sequential), known to stimulate autophagy. Autophagic activity increased in all experimental modalities, including both single agent and double agent exposures, and reached a steady state in all cases ~2 times control from ~8 to 24 hrs, suggesting the presence of an upper limit to autophagic capacity. These results are consistent with the hypothesis that environmental stressors might exert their harmful effects, at least in part, by limiting available autophagic response to additional stimulation, thereby making nanoparticle-exposed cells more susceptible to secondary injury due to autophagic overload.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10373127/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9945538","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

Topoisomerase I poisons-induced autophagy: Cytoprotective, Cytotoxic or Non-protective. 拓扑异构酶 I 毒物诱导的自噬：细胞保护作用、细胞毒性或无保护作用

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2022-12-25 DOI: 10.1080/27694127.2022.2155904

Ahmed M Elshazly, Polina A Wright, Jingwen Xu, David A Gewirtz

引用次数: 4

Shear stress induces autophagy in Schlemm's canal cells via primary cilia-mediated SMAD2/3 signaling pathway. 剪切应力通过初级纤毛介导的 SMAD2/3 信号通路诱导 Schlemm 管细胞自噬。

Autophagy reports Pub Date : 2023-01-01 Epub Date: 2023-07-20 DOI: 10.1080/27694127.2023.2236519

Myoung Sup Shim, Angela Dixon, April Nettesheim, Kristin M Perkumas, W Daniel Stamer, Yang Sun, Paloma B Liton

{"title":"Shear stress induces autophagy in Schlemm's canal cells via primary cilia-mediated SMAD2/3 signaling pathway.","authors":"Myoung Sup Shim, Angela Dixon, April Nettesheim, Kristin M Perkumas, W Daniel Stamer, Yang Sun, Paloma B Liton","doi":"10.1080/27694127.2023.2236519","DOIUrl":"10.1080/27694127.2023.2236519","url":null,"abstract":"The Schlemm's canal (SC) is a circular, lymphatic-like vessel located at the limbus of the eye that participates in the regulation of aqueous humor drainage to control intraocular pressure (IOP). Circumferential flow of aqueous humor within the SC lumen generates shear stress, which regulates SC cell behaviour. Using biochemical analysis and real-time live cell imaging techniques, we have investigated the activation of autophagy in SC cells by shear stress. We report, for the first time, the primary cilium (PC)-dependent activation of autophagy in SC cells in response to shear stress. Moreover, we identified PC-dependent shear stress-induced autophagy to be positively regulated by phosphorylation of SMAD2 in its linker and C-terminal regions. Additionally, SMAD2/3 signaling was found to transcriptionally activate LC3B, ATG5 and ATG7 in SC cells. Intriguingly, concomitant to SMAD2-dependent activation of autophagy, we also report here the activation of mTOR pathway, a classical autophagy inhibitor, in SC cells by shear stress. mTOR activation was found to also be dependent on the PC. Moreover, pharmacological inhibition of class I PI3K increased phosphorylation of SMAD2 at the linker and activated autophagy. Together, our data indicates an interplay between PI3K and SMAD2/3 signaling pathways in the regulation of PC-dependent shear stress-induced autophagy in SC cells.","PeriodicalId":72341,"journal":{"name":"Autophagy reports","volume":"2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10448710/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10492986","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