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Bianca Seminotti

Researcher at University of Pittsburgh

Publications -  4
Citations -  118

Bianca Seminotti is an academic researcher from University of Pittsburgh. The author has contributed to research in topics: Mitochondrion & Respiratory chain. The author has an hindex of 4, co-authored 4 publications receiving 78 citations. Previous affiliations of Bianca Seminotti include Universidade Federal do Rio Grande do Sul.

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Evaluation of mitochondrial bioenergetics, dynamics, endoplasmic reticulum-mitochondria crosstalk, and reactive oxygen species in fibroblasts from patients with complex I deficiency.

TL;DR: Treatment of ACAD9 deficient cells with JP4-039, a novel mitochondria-targeted reactive oxygen species, electron and radical scavenger, decreased superoxide level and increased basal and maximal respiratory rate is identified, identifying a potential therapeutic intervention opportunity in CI deficiency.
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Mitochondrial energetics is impaired in very long-chain acyl-CoA dehydrogenase deficiency and can be rescued by treatment with mitochondria-targeted electron scavengers.

TL;DR: The mitochondrially enriched electron and free radical scavengers JP4-039 and XJB-5-131 improved RC function and decreased ROS production significantly, suggesting that they are viable candidate compounds to further develop to treat VLCAD-deficient patients.
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ETHE1 and MOCS1 deficiencies: Disruption of mitochondrial bioenergetics, dynamics, redox homeostasis and endoplasmic reticulum-mitochondria crosstalk in patient fibroblasts

TL;DR: Data demonstrate that previously unrecognized broad disturbances of cellular function are involved in the pathophysiology of ETHE1 and MOCS1 deficiencies, and that reduction of mitochondrial superoxide by JP4-039 is a promising strategy for adjuvant therapy of these disorders.
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Reticular Dysgenesis and Mitochondriopathy Induced by Adenylate Kinase 2 Deficiency with Atypical Presentation.

TL;DR: It is demonstrated that reticular dysgenesis should be considered in Amish individuals presenting with immune deficiency and pathophysiological aspects of AK2 deficiency not previously reported are described.