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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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    Gut Microbiota‐Derived Extracellular Vesicles Influence Alcohol Intake Preferences in Rats
    (Wiley, 2025-03)
    Macarena Díaz‐Ubilla
    ;
    Aliosha I. Figueroa‐Valdés
    ;
    Hugo E. Tobar
    ;
    María Elena Quintanilla
    ;
    Eugenio Díaz
    <jats:title>ABSTRACT</jats:title><jats:p>Growing preclinical and clinical evidence suggests a link between gut microbiota dysbiosis and problematic alcohol consumption. Extracellular vesicles (EVs) are key mediators involved in bacteria‐to‐host communication. However, their potential role in mediating addictive behaviour remains unexplored. This study investigates the role of gut microbiota‐derived bacterial extracellular vesicles (bEVs) in driving high alcohol consumption. bEVs were isolated from the gut microbiota of a high alcohol‐drinking rat strain (UChB rats), either ethanol‐naïve or following chronic alcohol consumption and administered intraperitoneally or orally to alcohol‐rejecting male and female Wistar rats. Both types of UChB‐derived bEVs increased Wistar's voluntary alcohol consumption (three bottle choice test) up to 10‐fold (<jats:italic>p</jats:italic> &lt; 0.0001), indicating that bEVs are able and sufficient to transmit drinking behaviour across different rat strains. Molecular analysis revealed that bEVs administration did not induce systemic or brain inflammation in the recipient animals, suggesting that the increased alcohol intake triggered by UChB‐derived bEVs operates through an inflammation‐independent mechanism. Furthermore, we demonstrate that the vagus nerve mediates the bEV‐induced increase in alcohol consumption, as bilateral vagotomy completely abolished the high drinking behaviour induced by both intraperitoneally injected and orally administered bEVs. Thus, this study identifies bEVs as a novel mechanism underlying gut microbiota‐induced high alcohol intake in a vagus nerve‐dependent manner.</jats:p>
      7
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    Paw Skin as a Translational Model for Investigating Fibrotic and Inflammatory Wound Healing Defects in Recessive Dystrophic Epidermolysis Bullosa
    (MDPI AG, 2025-04-30)
    DE GREGORIO CONCHA, CRISTIAN ALEJANDRO  
    ;
    Giselle Ramos-Gonzalez
    ;
    Bernardo Morales-Catalán
    ;
    EZQUER, EDUARDO FERNANDO  
    ;
    EZQUER, EDUARDO MARCELO  
    Recessive dystrophic epidermolysis bullosa (RDEB) is a severe genetic disease caused by COL7A1 mutations. It leads to skin fragility, chronic inflammation, and impaired wound healing. The condition often results in fibrotic scarring, pseudosyndactyly, and cutaneous squamous cell carcinoma (SCC). However, current animal models fail to fully replicate chronic RDEB wounds. In this study, we used Collagen VII-hypomorphic mice (Col7a1flNeo/flNeo) and created full-thickness wounds on their paw skin, an area prone to fibrosis due to mechanical stress. We analyzed the healing process using histology, immunofluorescence, and electron microscopy. The RDEB mice showed delayed wound closure, increased inflammation, and poor granulation tissue formation. At 30 days post-injury, we observed persistent fibrosis, with elevated levels of Collagen I, α-SMA+ myofibroblasts, and tenascin-C. These mice also had fewer intraepidermal nerve fibers, which may help explain the neuropathic pain associated with RDEB. Our model reproduces the main features of chronic RDEB wounds. It offers a useful tool for evaluating therapies aimed at reducing inflammation, fibrosis, and tumor risk in these patients.
    Scopus© Citations 3  4
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    The Unexplored Role of Connexin Hemichannels in Promoting Facioscapulohumeral Muscular Dystrophy Progression
    (MDPI AG, 2025-01-04)
    Macarena Díaz-Ubilla
    ;
    RETAMAL LUCERO, MAURICIO ANTONIO  
    <jats:p>DUX4 is typically a repressed transcription factor, but its aberrant activation in Facioscapulohumeral Muscular Dystrophy (FSHD) leads to cell death by disrupting muscle homeostasis. This disruption affects crucial processes such as myogenesis, sarcolemma integrity, gene regulation, oxidative stress, immune response, and many other biological pathways. Notably, these disrupted processes have been associated, in other pathological contexts, with the presence of connexin (Cx) hemichannels—transmembrane structures that mediate communication between the intracellular and extracellular environments. Thus, hemichannels have been implicated in skeletal muscle atrophy, as observed in human biopsies and animal models of Duchenne Muscular Dystrophy, Becker Muscular Dystrophy, and Dysferlinopathies, suggesting a potentially shared mechanism of muscle atrophy that has not yet been explored in FSHD. Despite various therapeutic strategies proposed to manage FSHD, no treatment or cure is currently available. This review summarizes the current understanding of the mechanisms underlying FSHD progression, with a focus on hormones, inflammation, reactive oxygen species (ROS), and mitochondrial function. Additionally, it explores the potential of targeting hemichannels as a therapeutic strategy to slow disease progression by preventing the spread of pathogenic factors between muscle cells.</jats:p>
      5
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    Multiomics dissection of human RAG deficiency reveals distinctive patterns of immune dysregulation but a common inflammatory signature
    (American Association for the Advancement of Science (AAAS), 2025-01-10)
    Marita Bosticardo
    ;
    Kerry Dobbs
    ;
    Ottavia M. Delmonte
    ;
    Andrew J. Martins
    ;
    Francesca Pala
    <jats:p> Human recombination-activating gene (RAG) deficiency can manifest with distinct clinical and immunological phenotypes. By applying a multiomics approach to a large group of <jats:italic>RAG</jats:italic> -mutated patients, we aimed at characterizing the immunopathology associated with each phenotype. Although defective T and B cell development is common to all phenotypes, patients with hypomorphic <jats:italic>RAG</jats:italic> variants can generate T and B cells with signatures of immune dysregulation and produce autoantibodies to a broad range of self-antigens, including type I interferons. T helper 2 (T <jats:sub>H</jats:sub> 2) cell skewing and a prominent inflammatory signature characterize Omenn syndrome, whereas more hypomorphic forms of RAG deficiency are associated with a type 1 immune profile both in blood and tissues. We used cellular indexing of transcriptomes and epitopes by sequencing (CITE-seq) analysis to define the cell lineage–specific contribution to the immunopathology of the distinct RAG phenotypes. These insights may help improve the diagnosis and clinical management of the various forms of the disease. </jats:p>
    Scopus© Citations 2  1
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    Editorial: Immune response to gram-negative bacteria in the lungs
    (2024)
    Agnes Jara-Collao
    ;
    POLI HARLOWE, MARIA CECILIA BERTA  
    ;
    William Bain
    ;
    Hernán F. Peñaloza
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    Histiocitosis de Erdheim Chester como desafío diagnóstico ante un cuadro sistémico: Reporte de un caso
    (2024)
    Dominga García
    ;
    Yorman Flores
    ;
    Maximiliano Vergara
    ;
    Cristian Labarca Solar
    Scopus© Citations 1
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    Linoleic and Arachidonic Fatty Acids and their Potential Relationship
    with Inflammation, Pregnancy, and Fetal Development
    (2024)
    Macarena Ortiz
    ;
    Daniela Álvarez
    ;
    Yasna Muñoz
    ;
    Nicolás Crisosto
    ;
    Rodrigo Valenzuela
    <jats:sec> <jats:title>Abstract:</jats:title> <jats:p>A healthy maternal diet must consider an appropriate supply of long-chain polyunsaturated fatty acids (LCPUFAs) precursors to ensure adequate growth and development of the fetus. In this regard, n-6 PUFAs, predominantly linoleic (C18:2 n-6, LA) and arachidonic acid (C20:4 n-6), have a central role in the development of the central nervous system because they are part of the membrane structure and participate in the metabolism and signal transduction of cells. Nevertheless, they can also be transformed into inflammatory metabolites promoting the pathogenesis of cardiovascular diseases, cancer, and autoimmune or inflammatory conditions. In modern westernized societies, there is a high dietary consumption of foods rich in n-6 PUFAs which could have detrimental consequences for the fetus and neonate due to excessive exposure to these fatty acids (FAs).</jats:p> </jats:sec> <jats:sec> <jats:title>Objective:</jats:title> <jats:p>To summarize the evidence of maternal, placental, and fetal alterations that an excessive intake of n-6 polyunsaturated FAs (PUFAs), LA, and AA, could produce during pregnancy.</jats:p> </jats:sec> <jats:sec> <jats:title>Methods:</jats:title> <jats:p>A thorough review of the literature regarding the effects of n-6 PUFAs during pregnancy and lactation including in vivo and in vitro models, was carried out using the PubMed database from the National Library of Medicine-National Institutes of Health.</jats:p> </jats:sec> <jats:sec> <jats:title>Results:</jats:title> <jats:p>An elevated intake of n-6 PUFA, specifically LA, during pregnancy influences children's motor, cognitive, and verbal development during infancy and early childhood. Similarly, they could harm the placenta and the development of other fetal organs such as the fat tissue, liver, and cardiovascular system.</jats:p> </jats:sec> <jats:sec> <jats:title>Conclusion:</jats:title> <jats:p>Maternal diet, specifically LA intake, could have significant repercussions on fetal development and long-term consequences in the offspring, including the possibility of future metabolic and mental diseases. It would be necessary to focus on the prevention of these alterations through timely dietary interventions in the target population.</jats:p> </jats:sec>
    Scopus© Citations 6  11
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      2Scopus© Citations 22
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    Immunosensory signalling by carotid body chemoreceptors
    (2011)
    Patricio Zapata
    ;
    Carolina Larraín
    ;
    PABLO REYES P.
    ;
    Ricardo Fernández
      1Scopus© Citations 41