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Adherence to an Early Exercise Plan Promotes Visceral Fat Loss in the First Month Following Bariatric Surgery
(Springer Science and Business Media LLC, 2025-02-14)
Johanna Pino-Zuñiga
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Paloma Lillo-Urzua
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Mariela Olivares-Galvez
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Ana Palacio-Aguero
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Juan Camilo Duque
3Scopus© Citations 2
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Development of an artificial intelligence powered software for automated analysis of skeletal muscle ultrasonography
(Springer Science and Business Media LLC, 2025-04-29)
Zoe Calulo Rivera
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GONZALEZ SEGUEL, FELIPE ANDRES
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Arimitsu Horikawa-Strakovsky
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Catherine Granger
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Aarti Sarwal
1Scopus© Citations 11
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The Unexplored Role of Connexin Hemichannels in Promoting Facioscapulohumeral Muscular Dystrophy Progression
(MDPI AG, 2025-01-04)
Macarena Díaz-Ubilla
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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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Fibrotic response induced by angiotensin-II requires NAD(P)H oxidase-induced reactive oxygen species (ROS) in skeletal muscle cells
(2011)
Claudio Cabello-Verrugio
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María José Acuña
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María Gabriela Morales
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Alvaro Becerra
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Felipe Simon
Scopus© Citations 65 1
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Angiotensin II-induced pro-fibrotic effects require p38MAPK activity and transforming growth factor beta 1 expression in skeletal muscle cells
(2012)
María Gabriela Morales
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Yaneisi Vazquez
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María José Acuña
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Juan Carlos Rivera
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Felipe Simon
9Scopus© Citations 77
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Nutritional labeling and amino acid profile in high protein Chilean dairy products: a new alternative for health and sports
(2021)
Matías Monsalves Álvarez
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Alice Glaves Berhmann
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José Gómez-López
2Scopus© Citations 2
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Nutritional assessment by subjective methods versus computed tomography to predict survival in oncology patients
(2021)
Paula Von Geldern
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Claudio Salas
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Pablo Alvayay
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SILVA FUENTE ALBA, CLAUDIO SERGIO
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Maria Pía de la Maza
7Scopus© Citations 8
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Understanding the effect of window length and overlap for assessing sEMG in dynamic fatiguing contractions: A non-linear dimensionality reduction and clustering
(2021)
Carlos De la Fuente
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Eduardo Martinez-Valdes
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Jose Ignacio Priego-Quesada
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Alejandro Weinstein
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Oscar Valencia
Scopus© Citations 8 20
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Skeletal Muscle Atrophy Induced by Diabetes Is Mediated by Non-Selective Channels and Prevented by Boldine
(2023)
Luis A. Cea
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Walter Vásquez
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Romina Hernández-Salinas
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Alejandra Z. Vielma
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Mario Castillo-Ruiz
<jats:p>Individuals with diabetes mellitus present a skeletal muscle myopathy characterized by atrophy. However, the mechanism underlying this muscular alteration remains elusive, which makes it difficult to design a rational treatment that could avoid the negative consequences in muscles due to diabetes. In the present work, the atrophy of skeletal myofibers from streptozotocin-induced diabetic rats was prevented with boldine, suggesting that non-selective channels inhibited by this alkaloid are involved in this process, as has previously shown for other muscular pathologies. Accordingly, we found a relevant increase in sarcolemma permeability of skeletal myofibers of diabetic animals in vivo and in vitro due to de novo expression of functional connexin hemichannels (Cx HCs) containing connexins (Cxs) 39, 43, and 45. These cells also expressed P2X7 receptors, and their inhibition in vitro drastically reduced sarcolemma permeability, suggesting their participation in the activation of Cx HCs. Notably, sarcolemma permeability of skeletal myofibers was prevented by boldine treatment that blocks Cx43 and Cx45 HCs, and now we demonstrated that it also blocks P2X7 receptors. In addition, the skeletal muscle alterations described above were not observed in diabetic mice with myofibers deficient in Cx43/Cx45 expression. Moreover, murine myofibers cultured for 24 h in high glucose presented a drastic increase in sarcolemma permeability and levels of NLRP3, a molecular member of the inflammasome, a response that was also prevented by boldine, suggesting that, in addition to the systemic inflammatory response found in diabetes, high glucose can promote the expression of functional Cx HCs and activation of the inflammasome in skeletal myofibers. Therefore, Cx43 and Cx45 HCs play a critical role in myofiber degeneration, and boldine could be considered a potential therapeutic agent to treat muscular complications due to diabetes.</jats:p>
5Scopus© Citations 18
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Critical illness myopathy and trajectory of recovery in acute kidney injury requiring continuous renal replacement therapy: a prospective observational trial protocol
(2023)
J Pedro Teixeira
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Benjamin R Griffin
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Chaitanya Anil Pal
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David Felipe Márquez González
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Nathanial Jenkins
<jats:sec><jats:title>Introduction</jats:title><jats:p>Acute kidney injury requiring renal replacement therapy (AKI-RRT) is common in the intensive care unit (ICU) and is associated with significant morbidity and mortality. Continuous RRT (CRRT) non-selectively removes large amounts of amino acids from plasma, lowering serum amino acid concentrations and potentially depleting total-body amino acid stores. Therefore, the morbidity and mortality associated with AKI-RRT may be partly mediated through accelerated skeletal muscle atrophy and resulting muscle weakness. However, the impact of AKI-RRT on skeletal muscle mass and function during and following critical illness remains unknown. We hypothesise that patients with AKI-RRT have higher degrees of acute muscle loss than patients without AKI-RRT and that AKI-RRT survivors are less likely to recover muscle mass and function when compared with other ICU survivors.</jats:p></jats:sec><jats:sec><jats:title>Methods and analysis</jats:title><jats:p>This protocol describes a prospective, multicentre, observational trial assessing skeletal muscle size, quality and function in ICU patients with AKI-RRT. We will perform musculoskeletal ultrasound to longitudinally evaluate rectus femoris size and quality at baseline (within 48 hours of CRRT initiation), day 3, day 7 or at ICU discharge, at hospital discharge, and 1–3 months postdischarge. Additional skeletal muscle and physical function tests will be performed at hospital discharge and postdischarge follow-up. We will analyse the effect of AKI-RRT by comparing the findings in enrolled subjects to historical controls of critically ill patients without AKI-RRT using multivariable modelling.</jats:p></jats:sec><jats:sec><jats:title>Ethics and dissemination</jats:title><jats:p>We anticipate our study will reveal that AKI-RRT is associated with greater degrees of muscle loss and dysfunction along with impaired postdischarge recovery of physical function. These findings could impact the in-hospital and postdischarge treatment plan for these patients to include focused attention on muscle strength and function. We intend to disseminate findings to participants, healthcare professionals, the public and other relevant groups via conference presentation and publication without any publication restrictions.</jats:p></jats:sec><jats:sec><jats:title>Trial registration number</jats:title><jats:p><jats:ext-link xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="clintrialgov" xlink:href="NCT05287204">NCT05287204</jats:ext-link>.</jats:p></jats:sec>
4Scopus© Citations 5

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