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  1. Book ; Online: Autophagy: From Big Data to Physiological Significance

    Nezis, Ioannis / Sarkar, Sovan / Ines Vaccaro, Maria

    2020  

    Keywords Science: general issues ; Biology, life sciences ; autophagy ; xenophagy ; data ; disease ; screening
    Size 1 electronic resource (233 pages)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT021229932
    ISBN 9782889634828 ; 2889634825
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Metabolic function of autophagy is essential for cell survival.

    Sedlackova, Lucia / Kataura, Tetsushi / Sarkar, Sovan / Korolchuk, Viktor I

    Autophagy

    2023  Volume 19, Issue 8, Page(s) 2395–2397

    Abstract: Age-related human pathologies present with a multitude of molecular and metabolic phenotypes, which individually or synergistically contribute to tissue degeneration. However, current lack of understanding of the interdependence of these molecular ... ...

    Abstract Age-related human pathologies present with a multitude of molecular and metabolic phenotypes, which individually or synergistically contribute to tissue degeneration. However, current lack of understanding of the interdependence of these molecular pathologies limits the potential range of existing therapeutic intervention strategies. In our study, we set out to understand the chain of molecular events, which underlie the loss of cellular viability in macroautophagy/autophagy deficiency associated with aging and age-related disease. We discover a novel axis linking autophagy, a cellular waste disposal pathway, and a metabolite, nicotinamide adenine dinucleotide (NAD). The axis connects multiple organelles, molecules and stress response pathways mediating cellular demise when autophagy becomes dysfunctional. By elucidating the steps on the path from efficient mitochondrial recycling to NAD maintenance and ultimately cell viability, we highlight targets potentially receptive to therapeutic interventions in a range of genetic and age-related diseases associated with autophagy dysfunction.
    MeSH term(s) Humans ; Cell Survival ; Autophagy ; NAD/metabolism ; Mitochondria/metabolism ; Aging/metabolism ; Poly(ADP-ribose) Polymerases/metabolism
    Chemical Substances NAD (0U46U6E8UK) ; Poly(ADP-ribose) Polymerases (EC 2.4.2.30)
    Language English
    Publishing date 2023-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 2454135-7
    ISSN 1554-8635 ; 1554-8627
    ISSN (online) 1554-8635
    ISSN 1554-8627
    DOI 10.1080/15548627.2023.2165753
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Regulation of autophagy by mTOR-dependent and mTOR-independent pathways: autophagy dysfunction in neurodegenerative diseases and therapeutic application of autophagy enhancers.

    Sarkar, Sovan

    Biochemical Society transactions

    2013  Volume 41, Issue 5, Page(s) 1103–1130

    Abstract: Autophagy is an intracellular degradation pathway essential for cellular and energy homoeostasis. It functions in the clearance of misfolded proteins and damaged organelles, as well as recycling of cytosolic components during starvation to compensate for ...

    Abstract Autophagy is an intracellular degradation pathway essential for cellular and energy homoeostasis. It functions in the clearance of misfolded proteins and damaged organelles, as well as recycling of cytosolic components during starvation to compensate for nutrient deprivation. This process is regulated by mTOR (mammalian target of rapamycin)-dependent and mTOR-independent pathways that are amenable to chemical perturbations. Several small molecules modulating autophagy have been identified that have potential therapeutic application in diverse human diseases, including neurodegeneration. Neurodegeneration-associated aggregation-prone proteins are predominantly degraded by autophagy and therefore stimulating this process with chemical inducers is beneficial in a wide range of transgenic disease models. Emerging evidence indicates that compromised autophagy contributes to the aetiology of various neurodegenerative diseases related to protein conformational disorders by causing the accumulation of mutant proteins and cellular toxicity. Combining the knowledge of autophagy dysfunction and the mechanism of drug action may thus be rational for designing targeted therapy. The present review describes the cellular signalling pathways regulating mammalian autophagy and highlights the potential therapeutic application of autophagy inducers in neurodegenerative disorders.
    MeSH term(s) Autophagy/genetics ; Cell Survival/genetics ; Humans ; Molecular Targeted Therapy ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/genetics ; Neurodegenerative Diseases/pathology ; Signal Transduction ; Small Molecule Libraries/therapeutic use ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Small Molecule Libraries ; MTOR protein, human (EC 2.7.1.1) ; TOR Serine-Threonine Kinases (EC 2.7.1.1)
    Language English
    Publishing date 2013-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20130134
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: The autophagy-NAD axis in longevity and disease.

    Wilson, Niall / Kataura, Tetsushi / Korsgen, Miriam E / Sun, Congxin / Sarkar, Sovan / Korolchuk, Viktor I

    Trends in cell biology

    2023  Volume 33, Issue 9, Page(s) 788–802

    Abstract: Autophagy is an intracellular degradation pathway that recycles subcellular components to maintain metabolic homeostasis. NAD is an essential metabolite that participates in energy metabolism and serves as a substrate for a series of ... ...

    Abstract Autophagy is an intracellular degradation pathway that recycles subcellular components to maintain metabolic homeostasis. NAD is an essential metabolite that participates in energy metabolism and serves as a substrate for a series of NAD
    MeSH term(s) Animals ; NAD/metabolism ; Longevity ; Energy Metabolism ; NAD+ Nucleosidase/metabolism ; Autophagy
    Chemical Substances NAD (0U46U6E8UK) ; NAD+ Nucleosidase (EC 3.2.2.5)
    Language English
    Publishing date 2023-03-05
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2023.02.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3410: Show issues Location:
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  5. Article ; Online: Chemical screening platforms for autophagy drug discovery to identify therapeutic candidates for Huntington's disease and other neurodegenerative disorders.

    Sarkar, Sovan

    Drug discovery today. Technologies

    2013  Volume 10, Issue 1, Page(s) e137–44

    Abstract: Autophagy is a cellular degradation process involved in the clearance of aggregate-prone proteins associated with neurodegenerative diseases. While the mTOR pathway has been known to be the major regulator of autophagy, recent advancements into the ... ...

    Abstract Autophagy is a cellular degradation process involved in the clearance of aggregate-prone proteins associated with neurodegenerative diseases. While the mTOR pathway has been known to be the major regulator of autophagy, recent advancements into the regulation of autophagy have identified mTOR-independent autophagy pathways that are amenable to chemical perturbations. Several chemical and genetic screens have been undertaken to identify small molecule and genetic regulators of autophagy, respectively. The small molecule autophagy enhancers offer great potential as therapeutic candidates not only for neurodegenerative diseases, but also for diverse human diseases where autophagy acts as a protective pathway. This review highlights the various chemical screening platforms for autophagy drug discovery pertinent for the treatment of neurodegenerative diseases.
    MeSH term(s) Animals ; Autophagy ; Drug Discovery ; Humans ; Neurodegenerative Diseases/drug therapy
    Language English
    Publishing date 2013
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ISSN 1740-6749
    ISSN (online) 1740-6749
    DOI 10.1016/j.ddtec.2012.09.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: Editorial: Autophagy: From Big Data to Physiological Significance.

    Sarkar, Sovan / Vaccaro, Maria I / Nezis, Ioannis P

    Frontiers in cell and developmental biology

    2020  Volume 7, Page(s) 376

    Language English
    Publishing date 2020-01-10
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2019.00376
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Autophagy in Neurodegenerative Diseases.

    Korolchuk, Viktor I / Sarkar, Sovan / Fanto, Manolis

    Journal of molecular biology

    2020  Volume 432, Issue 8, Page(s) 2445–2448

    MeSH term(s) Animals ; Autophagy ; Humans ; Neurodegenerative Diseases/pathology
    Language English
    Publishing date 2020-03-10
    Publishing country England
    Document type Editorial
    ZDB-ID 80229-3
    ISSN 1089-8638 ; 0022-2836
    ISSN (online) 1089-8638
    ISSN 0022-2836
    DOI 10.1016/j.jmb.2020.03.005
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 867: Show issues Location:
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  8. Article ; Online: Autophagy in Rare (NonLysosomal) Neurodegenerative Diseases.

    Zatyka, Malgorzata / Sarkar, Sovan / Barrett, Timothy

    Journal of molecular biology

    2020  Volume 432, Issue 8, Page(s) 2735–2753

    Abstract: Neurodegenerative diseases (NDDs) comprise conditions with impaired neuronal function and loss and may be associated with a build-up of aggregated proteins with altered physicochemical properties (misfolded proteins). There are many disorders, and causes ...

    Abstract Neurodegenerative diseases (NDDs) comprise conditions with impaired neuronal function and loss and may be associated with a build-up of aggregated proteins with altered physicochemical properties (misfolded proteins). There are many disorders, and causes include gene mutations, infections, or exposure to toxins. The autophagy pathway is involved in the removal of unwanted proteins and organelles through lysosomes. While lysosomal storage disorders have been described for many years, it is now recognised that perturbations of the autophagy pathway itself can also lead to neurodegenerative disease. These include monogenic disorders of key proteins involved in the autophagy pathway, and disorders within pathways that critically control autophagy through monitoring of the supply of nutrients (mTORC1 pathway) or of energy supply in cells (AMPK pathway). This review focuses on childhood-onset neurodegenerative disorders with perturbed autophagy, due to defects in the autophagy pathway, or in upstream signalling via mTORC1 and AMPK. The review first provides a short description of autophagy, as related to neurons. It then examines the extended role of autophagy in neuronal function, plasticity, and memory. There follows a description of each step of the autophagy pathway in greater detail, illustrated with examples of diseases grouped by the stage of their perturbation of the pathway. Each disease is accompanied by a short clinical description, to illustrate the diversity but also the overlap of symptoms caused by perturbation of key proteins necessary for the proper functioning of autophagy. Finally, there is a consideration of current challenges that need addressing for future therapeutic advances.
    MeSH term(s) Animals ; Autophagy ; Humans ; Neurodegenerative Diseases/pathology ; Neurons/pathology ; Signal Transduction
    Language English
    Publishing date 2020-02-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80229-3
    ISSN 1089-8638 ; 0022-2836
    ISSN (online) 1089-8638
    ISSN 0022-2836
    DOI 10.1016/j.jmb.2020.02.012
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Autophagy Dysfunction as a Phenotypic Readout in hiPSC-Derived Neuronal Cell Models of Neurodegenerative Diseases.

    Sun, Congxin / Rosenstock, Tatiana R / Cohen, Malkiel A / Sarkar, Sovan

    Methods in molecular biology (Clifton, N.J.)

    2021  Volume 2549, Page(s) 103–136

    Abstract: Autophagy is an evolutionarily conserved catabolic pathway for the degradation of cytoplasmic constituents in eukaryotic cells. It is the primary disposal route for selective removal of undesirable cellular materials like aggregation-prone proteins and ... ...

    Abstract Autophagy is an evolutionarily conserved catabolic pathway for the degradation of cytoplasmic constituents in eukaryotic cells. It is the primary disposal route for selective removal of undesirable cellular materials like aggregation-prone proteins and damaged organelles for maintaining cellular homeostasis, and for bulk degradation of intracellular macromolecules and recycling the breakdown products for providing energy homeostasis during starvation. These functions of autophagy are attributed to cellular survival and thus pertinent for human health; however, malfunction of this process is detrimental to the cells, particularly for post-mitotic neurons. Thus, basal autophagy is vital for maintaining neuronal homeostasis, whereas autophagy dysfunction contributes to neurodegeneration. Defective autophagy has been demonstrated in several neurodegenerative diseases wherein pharmacological induction of autophagy is beneficial in many of these disease models. Elucidating the mechanisms underlying defective autophagy is imperative for the development of therapies targeting this process. Disease-affected human neuronal cells can be established from patient-derived human induced pluripotent stem cells (hiPSCs) that provide a clinically relevant platform for studying disease mechanisms and drug discovery. Thus, modeling autophagy dysfunction as a phenotypic readout in patient-derived neurons provides a more direct platform for investigating the mechanisms underlying defective autophagy and evaluating the therapeutic efficacy of autophagy inducers. Toward this, several hiPSC-derived neuronal cell models of neurodegenerative diseases have been employed. In this review, we highlight the key methodologies pertaining to hiPSC maintenance and neuronal differentiation, and studying autophagy at an endogenous level in hiPSC-derived neuronal cells.
    MeSH term(s) Autophagy ; Homeostasis ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Neurodegenerative Diseases/metabolism ; Neurons/metabolism
    Language English
    Publishing date 2021-09-08
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/7651_2021_420
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Analysis of Mitochondrial Dysfunction by Microplate Reader in hiPSC-Derived Neuronal Cell Models of Neurodegenerative Disorders.

    Rosenstock, Tatiana R / Sun, Congxin / Hughes, Georgina Wynne / Winter, Katherine / Sarkar, Sovan

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2549, Page(s) 1–21

    Abstract: Mitochondria are responsible for many vital pathways governing cellular homeostasis, including cellular energy management, heme biosynthesis, lipid metabolism, cellular proliferation and differentiation, cell cycle regulation, and cellular viability. ... ...

    Abstract Mitochondria are responsible for many vital pathways governing cellular homeostasis, including cellular energy management, heme biosynthesis, lipid metabolism, cellular proliferation and differentiation, cell cycle regulation, and cellular viability. Electron transport and ADP phosphorylation coupled with proton pumping through the mitochondrial complexes contribute to the preservation of mitochondrial membrane potential (ΔΨ
    MeSH term(s) Adenosine Diphosphate/metabolism ; Adenosine Triphosphate/metabolism ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Mitochondria/metabolism ; Neurodegenerative Diseases/metabolism ; Neurons/metabolism ; Reactive Oxygen Species/metabolism
    Chemical Substances Reactive Oxygen Species ; Adenosine Diphosphate (61D2G4IYVH) ; Adenosine Triphosphate (8L70Q75FXE)
    Language English
    Publishing date 2022-03-28
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/7651_2021_451
    Database MEDical Literature Analysis and Retrieval System OnLINE

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