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    A Narrative Review about Metabolic Pathways, Molecular Mechanisms and Clinical Implications of Intermittent Fasting as Autophagy Promotor
    (Springer Science and Business Media LLC, 2025-06-06)
    Álvaro Andrés Vergara Nieto
    ;
    Andrés Halabi Diaz
    ;
    Millaray Hernández
    ;
    Daniel Sagredo
      1
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    Neuronal Rubicon Represses Extracellular APP/Amyloid β Deposition in Alzheimer’s Disease
    (2022)
    Sandra Espinoza
    ;
    Felipe Grunenwald
    ;
    Wileidy Gomez
    ;
    Felipe García
    ;
    Lorena Abarzúa-Catalan  
    <jats:p>Alzheimer’s disease (AD) is the most prevalent age-associated neurodegenerative disease. A decrease in autophagy during aging contributes to brain disorders by accumulating potentially toxic substrates in neurons. Rubicon is a well-established inhibitor of autophagy in all cells. However, Rubicon participates in different pathways depending on cell type, and little information is currently available on neuronal Rubicon’s role in the AD context. Here, we investigated the cell-specific expression of Rubicon in postmortem brain samples from AD patients and 5xFAD mice and its impact on amyloid β burden in vivo and neuroblastoma cells. Further, we assessed Rubicon levels in human-induced pluripotent stem cells (hiPSCs), derived from early-to-moderate AD and in postmortem samples from severe AD patients. We found increased Rubicon levels in AD-hiPSCs and postmortem samples and a notable Rubicon localization in neurons. In AD transgenic mice lacking Rubicon, we observed intensified amyloid β burden in the hippocampus and decreased Pacer and p62 levels. In APP-expressing neuroblastoma cells, increased APP/amyloid β secretion in the medium was found when Rubicon was absent, which was not observed in cells depleted of Atg5, essential for autophagy, or Rab27a, required for exosome secretion. Our results propose an uncharacterized role of Rubicon on APP/amyloid β homeostasis, in which neuronal Rubicon is a repressor of APP/amyloid β secretion, defining a new way to target AD and other similar diseases therapeutically.</jats:p>
      5Scopus© Citations 4
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    The Autophagy Protein Pacer Positively Regulates the Therapeutic Potential of Mesenchymal Stem Cells in a Mouse Model of DSS-Induced Colitis
    (2022)
    Cristian A. Bergmann
    ;
    Sebastian Beltran
    ;
    Ana Maria Vega-Letter
    ;
    Paola Murgas
    ;
    Maria Fernanda Hernandez
    <jats:p>Mesenchymal stem cells (MSC) have emerged as a promising tool to treat inflammatory diseases, such as inflammatory bowel disease (IBD), due to their immunoregulatory properties. Frequently, IBD is modeled in mice by using dextran sulfate sodium (DSS)-induced colitis. Recently, the modulation of autophagy in MSC has been suggested as a novel strategy to improve MSC-based immunotherapy. Hence, we investigated a possible role of Pacer, a novel autophagy enhancer, in regulating the immunosuppressive function of MSC in the context of DSS-induced colitis. We found that Pacer is upregulated upon stimulation with the pro-inflammatory cytokine TNFα, the main cytokine released in the inflammatory environment of IBD. By modulating Pacer expression in MSC, we found that Pacer plays an important role in regulating the autophagy pathway in this cell type in response to TNFα stimulation, as well as in regulating the immunosuppressive ability of MSC toward T-cell proliferation. Furthermore, increased expression of Pacer in MSC enhanced their ability to ameliorate the symptoms of DSS-induced colitis in mice. Our results support previous findings that autophagy regulates the therapeutic potential of MSC and suggest that the augmentation of autophagic capacity in MSC by increasing Pacer levels may have therapeutic implications for IBD.</jats:p>
      4Scopus© Citations 12
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    Chaperone mediated autophagy contributes to the newly synthesized histones H3 and H4 quality control
    (2022)
    HORMAZABAL CASTILLO, JUAN PATRICIO  
    ;
    Francisco Saavedra
    ;
    Claudia Espinoza-Arratia
    ;
    Nicolas W Martinez
    ;
    Tatiana Cruces
    <jats:title>Abstract</jats:title> <jats:p>Although there are several pathways to ensure that proteins are folded properly in the cell, little is known about the molecular mechanisms regulating histone folding and proteostasis. In this work, we identified that chaperone-mediated autophagy (CMA) is the main pathway involved in the degradation of newly synthesized histones H3 and H4. This degradation is finely regulated by the interplay between HSC70 and tNASP, two histone interacting proteins. tNASP stabilizes histone H3 levels by blocking the direct transport of histone H3 into lysosomes. We further demonstrate that CMA degrades unfolded histone H3. Thus, we reveal that CMA is the main degradation pathway involved in the quality control of histone biogenesis, evidencing an additional mechanism in the intricate network of histone cellular proteostasis.</jats:p>
    Scopus© Citations 8  4
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      7Scopus© Citations 4
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    Scopus© Citations 14  3
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      32  1Scopus© Citations 12
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      35Scopus© Citations 149