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CHEMISTRY (537 journals)                  1 2 3 4 5 6 | Last

2D Materials     Hybrid Journal   (Followers: 3)
Accreditation and Quality Assurance: Journal for Quality, Comparability and Reliability in Chemical Measurement     Hybrid Journal   (Followers: 31)
ACS Catalysis     Full-text available via subscription   (Followers: 24)
ACS Chemical Neuroscience     Full-text available via subscription   (Followers: 13)
ACS Combinatorial Science     Full-text available via subscription   (Followers: 8)
ACS Macro Letters     Full-text available via subscription   (Followers: 17)
ACS Medicinal Chemistry Letters     Full-text available via subscription   (Followers: 25)
ACS Nano     Full-text available via subscription   (Followers: 270)
ACS Photonics     Full-text available via subscription   (Followers: 2)
ACS Synthetic Biology     Full-text available via subscription   (Followers: 8)
Acta Chemica Iasi     Open Access  
Acta Chimica Sinica     Full-text available via subscription  
Acta Chimica Slovaca     Open Access   (Followers: 6)
Acta Chromatographica     Full-text available via subscription   (Followers: 10)
Acta Facultatis Medicae Naissensis     Open Access   (Followers: 1)
Acta Metallurgica Sinica (English Letters)     Hybrid Journal   (Followers: 4)
adhäsion KLEBEN & DICHTEN     Hybrid Journal   (Followers: 3)
Adhesion Adhesives & Sealants     Hybrid Journal   (Followers: 4)
Adsorption Science & Technology     Full-text available via subscription   (Followers: 8)
Advanced Functional Materials     Hybrid Journal   (Followers: 34)
Advances in Chemical Engineering and Science     Open Access   (Followers: 21)
Advances in Chemical Science     Open Access   (Followers: 8)
Advances in Colloid and Interface Science     Full-text available via subscription   (Followers: 13)
Advances in Drug Research     Full-text available via subscription   (Followers: 17)
Advances in Fluorine Science     Full-text available via subscription   (Followers: 7)
Advances in Fuel Cells     Full-text available via subscription   (Followers: 12)
Advances in Heterocyclic Chemistry     Full-text available via subscription   (Followers: 8)
Advances in Materials Physics and Chemistry     Open Access   (Followers: 13)
Advances in Nanoparticles     Open Access   (Followers: 11)
Advances in Organometallic Chemistry     Full-text available via subscription   (Followers: 8)
Advances in Polymer Science     Hybrid Journal   (Followers: 38)
Advances in Protein Chemistry     Full-text available via subscription   (Followers: 6)
Advances in Protein Chemistry and Structural Biology     Full-text available via subscription   (Followers: 10)
Advances in Quantum Chemistry     Full-text available via subscription   (Followers: 4)
African Journal of Chemical Education     Open Access   (Followers: 1)
African Journal of Pure and Applied Chemistry     Open Access   (Followers: 4)
Afrique Science : Revue Internationale des Sciences et Technologie     Open Access  
Agrokémia és Talajtan     Full-text available via subscription   (Followers: 2)
Alchemy     Open Access   (Followers: 3)
Alkaloids: Chemical and Biological Perspectives     Full-text available via subscription   (Followers: 4)
AMB Express     Open Access   (Followers: 1)
American Journal of Applied Sciences     Open Access   (Followers: 28)
American Journal of Biochemistry and Biotechnology     Open Access   (Followers: 165)
American Journal of Biochemistry and Molecular Biology     Open Access   (Followers: 11)
American Journal of Chemistry     Open Access   (Followers: 17)
American Journal of Plant Physiology     Open Access   (Followers: 9)
American Mineralogist     Full-text available via subscription   (Followers: 2)
Analyst     Full-text available via subscription   (Followers: 35)
Angewandte Chemie     Hybrid Journal   (Followers: 16)
Angewandte Chemie International Edition     Hybrid Journal   (Followers: 213)
Annales UMCS, Chemia     Open Access   (Followers: 2)
Annual Reports in Computational Chemistry     Full-text available via subscription   (Followers: 1)
Annual Reports Section A (Inorganic Chemistry)     Full-text available via subscription   (Followers: 2)
Annual Reports Section B (Organic Chemistry)     Full-text available via subscription   (Followers: 4)
Annual Review of Chemical and Biomolecular Engineering     Full-text available via subscription   (Followers: 10)
Annual Review of Food Science and Technology     Full-text available via subscription   (Followers: 12)
Anti-Infective Agents     Hybrid Journal   (Followers: 1)
Applied Organometallic Chemistry     Hybrid Journal   (Followers: 4)
Applied Spectroscopy     Full-text available via subscription   (Followers: 12)
Applied Surface Science     Hybrid Journal   (Followers: 14)
Arabian Journal of Chemistry     Full-text available via subscription   (Followers: 6)
ARKIVOC     Open Access   (Followers: 1)
Asian Journal of Biochemistry     Open Access   (Followers: 1)
Australian Journal of Chemistry     Hybrid Journal   (Followers: 4)
Autophagy     Full-text available via subscription   (Followers: 1)
Avances en Quimica     Open Access   (Followers: 1)
Biochemical Pharmacology     Hybrid Journal   (Followers: 6)
Biochemistry     Full-text available via subscription   (Followers: 204)
Biochemistry Insights     Open Access   (Followers: 4)
Biochemistry Research International     Open Access   (Followers: 4)
BioChip Journal     Hybrid Journal   (Followers: 1)
Bioinorganic Chemistry and Applications     Open Access   (Followers: 4)
Biointerface Research in Applied Chemistry     Open Access   (Followers: 1)
Biointerphases     Open Access  
Biomacromolecules     Full-text available via subscription   (Followers: 17)
Biomass Conversion and Biorefinery     Partially Free   (Followers: 5)
Biomedical Chromatography     Hybrid Journal   (Followers: 7)
Biomolecular NMR Assignments     Hybrid Journal   (Followers: 2)
BioNanoScience     Partially Free   (Followers: 4)
Bioorganic & Medicinal Chemistry     Hybrid Journal   (Followers: 30)
Bioorganic & Medicinal Chemistry Letters     Hybrid Journal   (Followers: 24)
Bioorganic Chemistry     Hybrid Journal   (Followers: 5)
Biopolymers     Hybrid Journal   (Followers: 13)
Biosensors     Open Access   (Followers: 3)
Biotechnic and Histochemistry     Hybrid Journal   (Followers: 1)
Boletin de la Sociedad Chilena de Quimica     Open Access  
Bulletin of the Chemical Society of Ethiopia     Open Access   (Followers: 1)
Bulletin of the Chemical Society of Japan     Full-text available via subscription   (Followers: 12)
Canadian Association of Radiologists Journal     Full-text available via subscription   (Followers: 3)
Canadian Journal of Chemistry     Full-text available via subscription   (Followers: 6)
Canadian Mineralogist     Full-text available via subscription   (Followers: 1)
Carbohydrate Research     Hybrid Journal   (Followers: 10)
Carbon     Hybrid Journal   (Followers: 38)
Catalysis for Sustainable Energy     Open Access   (Followers: 2)
Catalysis Reviews: Science and Engineering     Hybrid Journal   (Followers: 4)
Catalysis Science and Technology     Free   (Followers: 4)
Catalysis Surveys from Asia     Hybrid Journal   (Followers: 4)
Catalysts     Open Access   (Followers: 6)
Cellulose     Hybrid Journal   (Followers: 4)
Central European Journal of Chemistry     Hybrid Journal   (Followers: 5)

        1 2 3 4 5 6 | Last

Journal Cover Autophagy
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     ISSN (Print) 1554-8627 - ISSN (Online) 1554-8635
     Published by Landes Bioscience Homepage  [34 journals]   [SJR: 2.31]   [H-I: 61]
  • Role of Epg5 in selective neurodegeneration and Vici syndrome
    • Abstract: Yan G. Zhao, Hongyu Zhao, Huayu Sun and Hong Zhang

      Autophagy activity is essential for the survival of neural cells. Impairment of autophagy has been implicated in the pathogenesis of neurodegenerative disorders. Unlike the massive neuron loss in mice deficient for autophagy genes essential for autophagosome formation, we demonstrated that mice deficient for the metazoan-specific autophagy gene Epg5 develop selective neuronal damage and exhibit key characteristics of amyotrophic lateral sclerosis. Epg5 deficiency blocks the maturation of autophagosomes into degradative autolysosomes, slows endocytic degradation and also impairs endocytic recycling. Recessive mutations in human EPG5 have recently been causally associated with the multisystem disorder Vici syndrome. Here we show that while Epg5 knockout mice display some features of Vici syndrome, many phenotypes are absent.
  • Autophagy: A key pathway of TNF-induced inflammatory bone loss
    • Abstract: Neng-Yu Lin, Adrian Stefanica and Jörg H.W. Distler

      Autophagy describes the degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery. Autophagy is essentially required to prevent accumulation of cellular damage and to ensure cellular homeostasis. Indeed, impaired autophagy has been implicated in a variety of different diseases. We examined the role of autophagy in inflammatory bone loss. We demonstrated that autophagy is activated by the pro-inflammatory cytokine tumor necrosis factor (TNF/TNFα) in osteoclasts of patients with rheumatoid arthritis (RA). Autophagy induces osteoclast differentiation and stimulates osteoclast-mediated bone resorption in vitro and in vivo, thereby highlighting autophagy as a novel mediator of TNF-induced bone resorption.
  • Autophagy receptor CALCOCO2/NDP52 takes center stage in Crohn disease
    • Abstract: Andreas Till, Simone Lipinski, David Ellinghaus, Gabriele Mayr, Suresh Subramani, Philip Rosenstiel and Andre Franke

      To advance understanding of the complex genetics of Crohn disease (CD) we sequenced 42 whole exomes of patients with CD and five healthy control individuals, resulting in identification of a missense mutation in the autophagy receptor calcium binding and coiled-coil domain 2 (CALCOCO2/NDP52) gene. Protein domain modeling and functional studies highlight the potential role of this mutation in controlling NFKB signaling downstream of toll-like receptor (TLR) pathways. We summarize our recent findings and discuss the role of autophagy as a major modulator of proinflammatory signaling in the context of chronic inflammation.
  • Tyrosine kinase inhibition facilitates autophagic SNCA/α-synuclein
    • Abstract: Michaeline L. Hebron, Irina Lonskaya and Charbel E.-H. Moussa

      The effects of ABL1/ABL inhibition on clearance of SNCA/α-synuclein were evaluated in animal models of α-synucleinopathies. Parkinson disease (PD) is a movement disorder characterized by death of dopaminergic substantia nigra (SN) neurons and brain accumulation of SNCA. The tyrosine kinase ABL1 is activated in several neurodegenerative diseases. An increase in ABL1 activity is detected in human postmortem PD brains. Lentiviral expression of SNCA in the mouse SN activates ABL1 via phosphorylation, while lentiviral Abl expression increases SNCA levels. Administration of the brain-penetrant tyrosine kinase inhibitor Nilotinib decreases Abl activity and facilitates autophagic clearance of SNCA in transgenic and lentiviral gene transfer models. Subcellular fractionation demonstrates accumulation of SNCA and hyperphosphorylated MAPT/Tau (p-MAPT) in autophagic vacuoles in SNCA-expressing brains, while Nilotinib treatment leads to protein deposition into the lysosomes, suggesting enhanced autophagic clearance. These data suggest that Nilotinib may be a therapeutic strategy to degrade SNCA in PD and other α-synucleinopathies.
  • A genetic model with specifically impaired autophagosome–lysosome
    • Abstract: Szabolcs Takáts and Gábor Juhász

      Yeast studies identified the evolutionarily conserved core ATG genes responsible for autophagosome formation. However, the SNARE-dependent machinery involved in autophagosome fusion with the vacuole in yeast is not conserved. We recently reported that the SNARE complex consisting of Syx17 (Syntaxin 17), ubisnap (SNAP-29) and Vamp7 is required for the fusion of autophagosomes with late endosomes and lysosomes in Drosophila. Syx17 mutant flies are viable but exhibit neuronal dysfunction, locomotion defects and premature death. These data point to the critical role of autophagosome clearance in organismal homeodynamics.
  • TFEB: Pathogenic role and therapeutic target in Parkinson disease
    • Abstract: Mickael Decressac and Anders Björklund

      Parkinson disease (PD) is characterized by the progressive loss of nigral dopamine neurons and the presence of accumulations containing the disease-causing protein SNCA/α-synuclein. Here we review our recent findings describing how SNCA impairs the function of the master regulator of the autophagy-lysosomal pathway (ALP), the transcription factor EB (TFEB), and that genetic or pharmacological stimulation of its activity promotes protection of dopamine neurons. These findings suggest that strategies aimed at enhancing autophagy-mediated degradation of SNCA may hold great promise for disease intervention in PD.
  • Autophagic degradation of leaf starch in plants
    • Abstract: Yan Wang and Yule Liu

      Autophagy is an evolutionarily conserved process in eukaryotic cells that functions to degrade cytoplasmic components in the vacuole or lysosome. Previous research indicates that the core molecular machinery of autophagosome formation works well in plants, and plant autophagy plays roles in diverse biological processes such as nutrient recycling, development, immunity and responses to a variety of abiotic stresses. Recently, we reported that autophagy contributed to leaf starch degradation, which had been thought to be a process confined to chloroplasts. This finding demonstrated a previously unidentified pathway of leaf starch depletion and a new role of basal autophagy in plants.
  • β-adrenergic receptor-stimulated lipolysis requires the RAB7-mediated
           autolysosomal lipid degradation
    • Abstract: Analyn Lizaso, Kien-Thiam Tan and Ying-Hue Lee

      Hormone-stimulated lipolysis is a rapid way to mobilize fat from its storage depot for use in peripheral tissues. By convention, activation of cytosolic lipases via the β-adrenergic receptor (ADRB2)-cAMP signaling pathway is the only molecular mechanism considered to liberate fatty acids from triglycerides stored in lipid droplets (LDs) of cells. Herein, we provide evidence that, aside from the activation of cytosolic lipases, autophagy contributes to this hormone-stimulated lipolysis. The ADRB2-stimulated lipolysis was reduced after inhibition of early or late autophagy using either pharmacological inhibitors or shRNA-mediated autophagic gene knockdown. ADRB2 stimulation has caused a marked increase in the autophagy-targeted LDs for lysosomal degradation, which is dependent on the LD-associated RAB7 as evidenced by the use of both shRNA-mediated RAB7 knockdown and a dominant-negative RAB7 mutant. In addition, RAB7 is involved in unstimulated (basal) lipolysis, and mediates the enhanced basal lipolysis in PLIN1/perilipin 1 knockdown fat cells. In conclusion, our results showed a contribution of lipophagy to both basal and hormone-stimulated lipolysis and that RAB7 plays a pivotal role in the regulation of this autolysosome-mediated lipid degradation in fat cells.
  • Drosophila Fip200 is an essential regulator of autophagy that attenuates
           both growth and aging
    • Abstract: Myungjin Kim, Hae Li Park, Hwan-Woo Park, Seung-Hyun Ro, Samuel G. Nam, John M. Reed, Jun-Lin Guan and Jun Hee Lee

      Autophagy-related 1 (Atg1)/Unc-51-like protein kinases (ULKs) are evolutionarily conserved proteins that play critical physiological roles in controlling autophagy, cell growth and neurodevelopment. RB1-inducible coiled-coil 1 (RB1CC1), also known as PTK2/FAK family-interacting protein of 200 kDa (FIP200) is a recently discovered binding partner of ULK1. Here we isolated the Drosophila RB1CC1/FIP200 homolog (Fip200/CG1347) and showed that it mediates Atg1-induced autophagy as a genetically downstream component in diverse physiological contexts. Fip200 loss-of-function mutants experienced severe mobility loss associated with neuronal autophagy defects and neurodegeneration. The Fip200 mutants were also devoid of both developmental and starvation-induced autophagy in salivary gland and fat body, while having no defects in axonal transport and projection in developing neurons. Interestingly, moderate downregulation of Fip200 accelerated both developmental growth and aging, accompanied by target of rapamycin (Tor) signaling upregulation. These results suggest that Fip200 is a critical downstream component of Atg1 and specifically mediates Atg1’s autophagy-, aging- and growth-regulating functions.
  • IκB kinase complex (IKK) triggers detachment-induced autophagy in
           mammary epithelial cells independently of the PI3K-AKT-MTORC1 pathway
    • Abstract: Nan Chen and Jayanta Debnath

      Adherent cells require proper integrin-mediated extracellular matrix (ECM) engagement for growth and survival; normal cells deprived of proper ECM contact undergo anoikis. At the same time, autophagy is induced as a survival pathway in both fibroblasts and epithelial cells upon ECM detachment. Here, we further define the intracellular signals that mediate detachment-induced autophagy and uncover an important role for the IκB kinase (IKK) complex in the induction of autophagy in mammary epithelial cells (MECs) deprived of ECM contact. Whereas the PI3K-AKT-MTORC1 pathway activation potently inhibits autophagy in ECM-detached fibroblasts, enforced activation of this pathway is not sufficient to suppress detachment-induced autophagy in MECs. Instead, inhibition of IKK, as well as its upstream regulator, MAP3K7/TAK1, significantly attenuates detachment-induced autophagy in MECs. Furthermore, function-blocking experiments corroborate that both IKK activation and autophagy induction result from decreased ITGA3-ITGB1 (α3β1 integrin) function. Finally, we demonstrate that pharmacological IKK inhibition enhances anoikis and accelerates luminal apoptosis during acinar morphogenesis in three-dimensional culture. Based on these results, we propose that the IKK complex functions as a key mediator of detachment-induced autophagy and anoikis resistance in epithelial cells.
  • ATG4B/autophagin-1 regulates intestinal homeostasis and protects mice from
           experimental colitis
    • Abstract: Sandra Cabrera, Álvaro F. Fernández, Guillermo Mariño, Alina Aguirre, María F. Suárez, Yaiza Español, José A. Vega, Rosaria Laurà, Antonio Fueyo, M. Soledad Fernández-García, José M.P. Freije, Guido Kroemer and Carlos López-Otín

      The identification of inflammatory bowel disease (IBD) susceptibility genes by genome-wide association has linked this pathology to autophagy, a lysosomal degradation pathway that is crucial for cell and tissue homeostasis. Here, we describe autophagy-related 4B, cysteine peptidase/autophagin-1 (ATG4B) as an essential protein in the control of inflammatory response during experimental colitis. In this pathological condition, ATG4B protein levels increase in parallel with the induction of autophagy. Moreover, ATG4B expression is significantly reduced in affected areas of the colon from IBD patients. Consistently, atg4b−/− mice present Paneth cell abnormalities, as well as an increased susceptibility to DSS-induced colitis. atg4b-deficient mice exhibit significant alterations in proinflammatory cytokines and mediators of the immune response to bacterial infections, which are reminiscent of those found in patients with Crohn disease or ulcerative colitis. Additionally, antibiotic treatments and bone marrow transplantation from wild-type mice reduced colitis in atg4b−/− mice. Taken together, these results provided additional evidence for the importance of autophagy in intestinal pathologies and describe ATG4B as a novel protective protein in inflammatory colitis. Finally, we propose that atg4b-null mice are a suitable model for in vivo studies aimed at testing new therapeutic strategies for intestinal diseases associated with autophagy deficiency.
  • 20-hydroxyecdysone upregulates Atg genes to induce autophagy in the Bombyx
           fat body
    • Abstract: Ling Tian, Li Ma, Enen Guo, Xiaojuan Deng, Sanyuan Ma, Qingyou Xia, Yang Cao and Sheng Li

      Autophagy is finely regulated at multiple levels and plays crucial roles in development and disease. In the fat body of the silkworm, Bombyx mori, autophagy occurs and Atg gene expression peaks during the nonfeeding molting and pupation stages when the steroid hormone (20-hydroxyecdysone; 20E) is high. Injection of 20E into the feeding larvae upregulated Atg genes and reduced TORC1 activity resulting in autophagy induction in the fat body. Conversely, RNAi knockdown of the 20E receptor partner (USP) or targeted overexpression of a dominant negative mutant of the 20E receptor (EcRDN) in the larval fat body reduced autophagy and downregulated the Atg genes, confirming the importance of 20E-induction of Atg gene expression during pupation. Moreover, in vitro treatments of the larval fat body with 20E upregulated the Atg genes. Five Atg genes were potentially 20E primary-responsive, and a 20E response element was identified in the Atg1 (ortholog of human ULK1) promoter region. Furthermore, RNAi knockdown of 4 key genes (namely Br-C, E74, HR3 and βftz-F1) in the 20E-triggered transcriptional cascade reduced autophagy and downregulated Atg genes to different levels. Taken together, we conclude that in addition to blocking TORC1 activity for autophagosome initiation, 20E upregulates Atg genes to induce autophagy in the Bombyx fat body.
  • Amorphous areas in the cytoplasm of Dendrobium tepal cells: Production
    • Abstract: Wouter G. van Doorn, Kanjana Kirasak and Saichol Ketsa

      In Dendrobium flowers some tepal mesophyll cells showed cytoplasmic areas devoid of large organelles. Such amorphous areas comprised up to about 40% of the cross-section of a cell. The areas were not bound by a membrane. The origin of these areas is not known. We show data suggesting that they can be formed from vesicle-like organelles. The data imply that these organelles and other material become degraded inside the cytoplasm. This can be regarded as a form of autophagy. The amorphous areas became surrounded by small vacuoles, vesicles or double membranes. These seemed to merge and thereby sequester the areas. Degradation of the amorphous areas therefore seemed to involve macroautophagy.
  • Direct uptake and degradation of DNA by lysosomes
    • Abstract: Yuuki Fujiwara, Hisae Kikuchi, Shu Aizawa, Akiko Furuta, Yusuke Hatanaka, Chiho Konya, Kenko Uchida, Keiji Wada and Tomohiro Kabuta

      Lysosomes contain various hydrolases that can degrade proteins, lipids, nucleic acids and carbohydrates. We recently discovered “RNautophagy,” an autophagic pathway in which RNA is directly taken up by lysosomes and degraded. A lysosomal membrane protein, LAMP2C, a splice variant of LAMP2, binds to RNA and acts as a receptor for this pathway. In the present study, we show that DNA is also directly taken up by lysosomes and degraded. Like RNautophagy, this autophagic pathway, which we term “DNautophagy,” is dependent on ATP. The cytosolic sequence of LAMP2C also directly interacts with DNA, and LAMP2C functions as a receptor for DNautophagy, in addition to RNautophagy. Similarly to RNA, DNA binds to the cytosolic sequences of fly and nematode LAMP orthologs. Together with the findings of our previous study, our present findings suggest that RNautophagy and DNautophagy are evolutionarily conserved systems in Metazoa.
  • The CFATG (Club Francophone de l’Autophagie, or The Francophone
           Autophagy Club)
    • Abstract:

  • Functions of autophagy in normal and diseased liver
    • Abstract: Mark J. Czaja, Wen-Xing Ding, Terrence M. Donohue, Scott L. Friedman, Jae-Sung Kim, Masaaki Komatsu, John J. Lemasters, Antoinette Lemoine, Jiandie D. Lin, Jing-hsiung James Ou, David H. Perlmutter, Glenn Randall, Ratna B. Ray, Allan Tsung and Xiao-Ming Yin

      Autophagy has emerged as a critical lysosomal pathway that maintains cell function and survival through the degradation of cellular components such as organelles and proteins. Investigations specifically employing the liver or hepatocytes as experimental models have contributed significantly to our current knowledge of autophagic regulation and function. The diverse cellular functions of autophagy, along with unique features of the liver and its principal cell type the hepatocyte, suggest that the liver is highly dependent on autophagy for both normal function and to prevent the development of disease states. However, instances have also been identified in which autophagy promotes pathological changes such as the development of hepatic fibrosis. Considerable evidence has accumulated that alterations in autophagy are an underlying mechanism of a number of common hepatic diseases including toxin-, drug- and ischemia/reperfusion-induced liver injury, fatty liver, viral hepatitis and hepatocellular carcinoma. This review summarizes recent advances in understanding the roles that autophagy plays in normal hepatic physiology and pathophysiology with the intent of furthering the development of autophagy-based therapies for human liver diseases.
  • The intense gravitational attraction of autophagy
    • Abstract: Daniel J. Klionsky

      In the course of my work as Autophagy editor, I try to gauge the overall patterns of interest in autophagy research. Not surprisingly, the number of papers associated with this topic has increased steadily. However, that trend provides only one glimpse into the way interest in this field has been changing—that the number of people working on autophagy has expanded. Perhaps not surprisingly, the number of different research areas that now include autophagy studies is also increasing. Thus, I decided to carry out an informal, imprecise analysis of the number of different journals (presumably reflecting in part the number of topics) that include papers on autophagy.
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