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Maria Svelto

Researcher at University of Bari

Publications -  197
Citations -  8331

Maria Svelto is an academic researcher from University of Bari. The author has contributed to research in topics: Aquaporin & Water transport. The author has an hindex of 52, co-authored 188 publications receiving 7471 citations. Previous affiliations of Maria Svelto include University of Basilicata.

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Journal ArticleDOI

The inner mitochondrial membrane has aquaporin-8 water channels and is highly permeable to water.

TL;DR: The presence of a member of the aquaporin family of water channels, AQP8, is shown and the strikingly high water permeability (Pf) characterizing the rat liver IMM is demonstrated, suggesting that AQP 8-mediated water transport may be particularly important for rapid expansions of mitochondrial volume.
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The role of aquaporin-4 in the blood-brain barrier development and integrity: studies in animal and cell culture models.

TL;DR: The purpose of this work is to integrate previous and recent data regarding AQP4 expression during BBB formation and depending on BBB integrity, using several experimental models.
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Aquaporin-4 deficiency in skeletal muscle and brain of dystrophic mdx mice

TL;DR: Evidence is provided that dystrophin deficiency in mdx mice leads to disturbances in AQP4 assembly in the plasma membrane of fast skeletal muscle fibers and brain astrocytic end‐feet, suggesting that changes in the osmotic equilibrium of the neuromuscular apparatus may be involved in the pathology of muscular dystrophy.
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Expression of aquaporin-4 in fast-twitch fibers of mammalian skeletal muscle.

TL;DR: Evidence is provided for the first time evidence for the expression of an aquaporin in skeletal muscle correlated to a specific fiber-type metabolism and a marked reduction of AQP4 expression suggesting a critical role in the membrane alteration of Duchenne muscular dystrophy.
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Severe alterations of endothelial and glial cells in the blood‐brain barrier of dystrophic mdx mice

TL;DR: The findings indicate that dystrophin deficiency in the mdx brain leads to severe injury of the endothelial and glial cells with disturbance in α‐actin cytoskeleton, ZO‐1, claudin‐ 1, and AQP4 assembly, as well as BBB breakdown.