Publicacións nas que colabora con Paula Cilleros Holgado (12)

2023

  1. Actin Polymerization Defects Induce Mitochondrial Dysfunction in Cellular Models of Nemaline Myopathies

    Antioxidants, Vol. 12, Núm. 12

  2. Alpha-lipoic acid supplementation corrects pathological alterations in cellular models of pantothenate kinase-associated neurodegeneration with residual PANK2 expression levels

    Orphanet journal of rare diseases, Vol. 18, Núm. 1, pp. 80

  3. Antioxidants Prevent Iron Accumulation and Lipid Peroxidation, but Do Not Correct Autophagy Dysfunction or Mitochondrial Bioenergetics in Cellular Models of BPAN

    International Journal of Molecular Sciences, Vol. 24, Núm. 19

  4. Mitochondrial Quality Control via Mitochondrial Unfolded Protein Response (mtUPR) in Ageing and Neurodegenerative Diseases

    Biomolecules, Vol. 13, Núm. 12

  5. Neurodegeneration, Mitochondria, and Antibiotics

    Metabolites, Vol. 13, Núm. 3

  6. Patient-Derived Cellular Models for Polytarget Precision Medicine in Pantothenate Kinase-Associated Neurodegeneration

    Pharmaceuticals, Vol. 16, Núm. 10

  7. Vicious cycle of lipid peroxidation and iron accumulation in neurodegeneration

    Neural Regeneration Research, Vol. 18, Núm. 6, pp. 1196-1202

  8. mtUPR Modulation as a Therapeutic Target for Primary and Secondary Mitochondrial Diseases

    International Journal of Molecular Sciences, Vol. 24, Núm. 2

2022

  1. Activation of the Mitochondrial Unfolded Protein Response: A New Therapeutic Target?

    Biomedicines, Vol. 10, Núm. 7

  2. Pantothenate and L-Carnitine Supplementation Improves Pathological Alterations in Cellular Models of KAT6A Syndrome

    Genes, Vol. 13, Núm. 12

  3. Therapeutic approach with commercial supplements for pantothenate kinase-associated neurodegeneration with residual PANK2 expression levels

    Orphanet journal of rare diseases, Vol. 17, Núm. 1, pp. 311

  4. UPRmt activation improves pathological alterations in cellular models of mitochondrial diseases

    Orphanet Journal of Rare Diseases, Vol. 17, Núm. 1