Ariz Galilea, Mikel
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Ariz Galilea
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Mikel
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Ingeniería Eléctrica, Electrónica y de Comunicación
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ISC. Institute of Smart Cities
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Publication Open Access Muscular and tendon degeneration after Achilles rupture: new insights into future repair strategies(MDPI, 2022) Gil-Melgosa, Lara; Grasa, Jorge; Urbiola, Ainhoa; Llombart, Rafael; Susaeta Ruiz, Miguel; Montiel, Verónica; Ederra, Cristina; Calvo, Begoña; Ariz Galilea, Mikel; Ripalda-Cemborain, Purificación; Prósper, Felipe; Ortiz de Solórzano, Carlos; Pons-Villanueva, Juan; Pérez Ruiz, Ana; Ingeniería Eléctrica, Electrónica y de Comunicación; Ingeniaritza Elektrikoa, Elektronikoa eta Telekomunikazio IngeniaritzaAchilles tendon rupture is a frequent injury with an increasing incidence. After clinical surgical repair, aimed at suturing the tendon stumps back into their original position, the repaired Achilles tendon is often plastically deformed and mechanically less strong than the pre-injured tissue, with muscle fatty degeneration contributing to function loss. Despite clinical outcomes, pre-clinical research has mainly focused on tendon structural repair, with a lack of knowledge regarding injury progression from tendon to muscle and its consequences on muscle degenerative/regenerative processes and function. Here, we characterize the morphological changes in the tendon, the myotendinous junction and muscle belly in a mouse model of Achilles tendon complete rupture, finding cellular and fatty infiltration, fibrotic tissue accumulation, muscle stem cell decline and collagen fiber disorganization. We use novel imaging technologies to accurately relate structural alterations in tendon fibers to pathological changes, which further explain the loss of muscle mechanical function after tendon rupture. The treatment of tendon injuries remains a challenge for orthopedics. Thus, the main goal of this study is to bridge the gap between clinicians’ knowledge and research to address the underlying pathophysiology of ruptured Achilles tendon and its consequences in the gastrocnemius. Such studies are necessary if current practices in regenerative medicine for Achilles tendon ruptures are to be improved.Publication Open Access Astrocytic GLUT1 reduction paradoxically improves central and peripheral glucose homeostasis(American Association for the Advancement of Science, 2024-10-18) Ardanaz, Carlos G.; Cruz, Aida de la; Minhas, Paras S.; Hernández-Martín, Nira; Pozo, Miguel Ángel ; Valdecantos, M. Pilar; Martínez Valverde, Ángela; Villa-Valverde, Palmira; Elizalde-Horcada, Marcos; Puerta, Elena; Ramírez, María J.; Ortega, Jorge E.; Urbiola, Ainhoa; Ederra, Cristina; Ariz Galilea, Mikel; Ortiz de Solórzano, Carlos; Fernández Irigoyen, Joaquín; Santamaría Martínez, Enrique; Karsenty, Gerard; Brüning, Jens C. ; Solas, Maite; Ciencias de la Salud; Osasun Zientziak; Ingeniería Eléctrica, Electrónica y de Comunicación; Ingeniaritza Elektrikoa, Elektronikoa eta Telekomunikazio IngeniaritzaAstrocytes are considered an essential source of blood-borne glucose or its metabolites to neurons. Nonetheless, the necessity of the main astrocyte glucose transporter, i.e., GLUT1, for brain glucose metabolism has not been defined. Unexpectedly, we found that brain glucose metabolism was paradoxically augmented in mice with astrocytic GLUT1 reduction (GLUT1ΔGFAP mice). These mice also exhibited improved peripheral glucose metabolism especially in obesity, rendering them metabolically healthier. Mechanistically, we observed that GLUT1-deficient astrocytes exhibited increased insulin receptor–dependent ATP release, and that both astrocyte insulin signaling and brain purinergic signaling are essential for improved brain function and systemic glucose metabolism. Collectively, we demonstrate that astrocytic GLUT1 is central to the regulation of brain energetics, yet its depletion triggers a reprogramming of brain metabolism sufficient to sustain energy requirements, peripheral glucose homeostasis, and cognitive function.