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Profil bibliographique

Paola Cavalcante

Informations fournies par OpenAlex. Research Africa ne déduit ni nationalité, ni poste, ni coordonnées personnelles.

82Publications signalées
2476Citations signalées
1Affiliations récentes

Les institutions déclarées

Les domaines associés

Myasthenia Gravis and ThymomaPeripheral Neuropathies and DisordersAmyotrophic Lateral Sclerosis ResearchNeurogenetic and Muscular Disorders ResearchAdrenal Hormones and Disorders

Les publications récentes

Accès ouvert 2026 article OpenAlex

Possible involvement of viral infection in the pathogenesis of myasthenia gravis

Maria Dolci, Lucia Signorini, Federica Perego, Sara Passerini et autres

Myasthenia gravis (MG) is a chronic autoimmune disorder that involves the targeting of neuromuscular junctions and is primarily driven by autoantibodies against the acetylcholine receptor (AChR). While genetic susceptibility is a factor, environmental triggers, particularly viral infections, are being increasingly investigated as …

it (code pays fourni par la source)

0 citations Journal of NeuroVirology
Accès ouvert 2026 article OpenAlex

Therapeutic inhibition of telomeric DNA damage response rescues hematopoietic dysfunction driven by telomere shortening and aging

Alessia Oppezzo, Sara Sepe, Giada Cicio, Valeria Cancila et autres

Telomeres progressively shorten and accumulate damage with aging, and this contributes to cellular senescence and hematopoietic dysfunction. We previously showed that telomere dysfunction induces synthesis of telomeric noncoding RNAs required for activation of the telomeric DNA damage response (tDDR), a driver of …

it, in, ru (code pays fourni par la source)

2 citations Nature Aging
Accès ouvert 2026 dataset OpenAlex

Dataset related to article: Unknown Immunoregulatory Effects of FcRn Inhibition by Efgartigimod in Myasthenia Gravis: A New Mechanism of Action Beyond IgG Reduction

Maria Cristina Tarasco, Elena Rinaldi, RITA FRANGIAMORE, Fiammetta Vanoli et autres

Raw data derived by immunological and molecular analyses performed in myasthenia gravis (MG) patients treated with efgartigimod, an FcRn inhibitor drug, including: i) serum IgG and autoAb quantification by ELISA and RIA; ii) circulating T- and B-cell subpopulation analysis by flow cytometry; …

it (code pays fourni par la source)

0 citations Zenodo (CERN European Organization for Nuclear Research)
Accès ouvert 2026 dataset OpenAlex

Dataset related to article: Unknown Immunoregulatory Effects of FcRn Inhibition by Efgartigimod in Myasthenia Gravis: A New Mechanism of Action Beyond IgG Reduction

Maria Cristina Tarasco, Elena Rinaldi, RITA FRANGIAMORE, Fiammetta Vanoli et autres

Raw data derived by immunological and molecular analyses performed in myasthenia gravis (MG) patients treated with efgartigimod, an FcRn inhibitor drug, including: i) serum IgG and autoAb quantification by ELISA and RIA; ii) circulating T- and B-cell subpopulation analysis by flow cytometry; …

it (code pays fourni par la source)

0 citations Zenodo (CERN European Organization for Nuclear Research)
Accès ouvert 2026 article OpenAlex

MicroRNA profiling in post-mortem spinal cord of C9ORF72-related ALS patients reveals molecular pathways involved in motor neuron degeneration

Giorgia Farinazzo, Eleonora Giagnorio, Matteo Marcuzzo, Marco Cattaneo et autres

Introduction: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder causing progressive motor neuron death in cortex, brainstem and spinal cord. The most common genetic cause is the G4C2 hexanucleotide repeat expansion in the non-coding region of exon 1 of C9ORF72, accounting …

it (code pays fourni par la source)

0 citations Frontiers in Neuroscience
Accès ouvert 2025 article OpenAlex

Profibrotic Molecules Are Reduced in CRISPR-Edited Emery–Dreifuss Muscular Dystrophy Fibroblasts

Eleonora Cattin, Elisa Schena, Elisabetta Mattioli, Stefania Marcuzzo et autres

Emery–Dreifuss muscular dystrophy (EDMD) is caused by mutations in EMD, LMNA, SYNE1, SYNE2, and other related genes. The disease is characterized by joint contractures, muscle weakening and wasting, and heart conduction defects associated with dilated cardiomyopathy. Previous studies demonstrated the activation of …

it, gb (code pays fourni par la source)

2 citations Cells
Accès ouvert 2025 article OpenAlex

Unknown Immunoregulatory Effects of FcRn Inhibition by Efgartigimod in Myasthenia Gravis

Maria Cristina Tarasco, Elena Rinaldi, Rita Frangiamore, Fiammetta Vanoli et autres

BACKGROUND AND OBJECTIVES: Efgartigimod (EFG), a biological drug targeting the IgG recycling neonatal Fc receptor (FcRn), leads to clinical improvements in patients affected by myasthenia gravis (MG), a prototypic autoantibody (Ab)-mediated autoimmune disease affecting neuromuscular junction. Because FcRn is a multifunctional protein …

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20 citations Neurology Neuroimmunology & Neuroinflammation
Accès ouvert 2025 article OpenAlex

Anti-myogenic and profibrotic effect of serum from patients affected by muscular laminopathies.

Elisa Schena, Antonella Pini, Paola Cavalcante, Gabriele Siciliano et autres

Emery-Dreifuss Muscular Dystrophy type 2 (EDMD2) and LMNA-related congenital muscular dystrophy (L-CMD) are caused by mutations in LMNA gene. Both pathologies are characterized by joint contractures, muscle weakness and wasting and cardiac involvement. In the last few years, circulating factors have been …

it (code pays fourni par la source)

0 citations PubMed
Accès ouvert 2025 article OpenAlex

Baricitinib and Lonafarnib Synergistically Target Progerin and Inflammation, Improving Lifespan and Health in Progeria Mice

Peter Krüger, Moritz Schroll, Felix Quirin Fenzl, Ramona Hartinger et autres

Hutchinson–Gilford progeria syndrome (HGPS) is a rare, fatal, and premature aging disorder caused by progerin, a truncated form of lamin A that disrupts nuclear architecture, induces systemic inflammation, and accelerates senescence. While the farnesyltransferase inhibitor lonafarnib extends the lifespan by limiting progerin …

de, us, it (code pays fourni par la source)

5 citations International Journal of Molecular Sciences

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