Joanna Fiddler
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Assistant Professor
Also affiliated: Oklahoma State University (2014–2021); Cornell University (2018–2024); Clemson University (2023–2025)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Joanna Fiddler's research investigates the molecular mechanisms underlying mitochondrial dysfunction and its impact on cellular processes. Her work has focused on the role of folate metabolism in mitochondrial health, examining how deficiencies in enzymes like SHMT2 affect mitochondrial respiration, uracil accumulation in mitochondrial DNA, and overall cellular energy production. Fiddler has also explored the effects of specific nutrients, such as vitamin B12 and folic acid, on mitochondrial heteroplasmy in animal models. Further research has examined the link between selective serotonin reuptake inhibitors and cardiac toxicity, identifying mitochondrial and sarcomere dysfunction as key contributors. Her studies have employed various model organisms, including mice and rats, and have utilized techniques to assess cellular metabolism and gene expression in response to dietary deficiencies and pharmacological agents. Fiddler has published 32 papers, with an h-index of 6 and 116 total citations, and collaborates with researchers at the University of Arkansas at Fayetteville.
Metrics
- h-index: 7
- Publications: 32
- Citations: 121
Selected Publications
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Transient MYC Mimicking the Exercise Response Orchestrates Multifaceted Skeletal Muscle Adaptations (2026)
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Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver (2025)
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Loss of SHMT2 and Folate Deficiency Impair Protein Levels Involved in Oxidative Phosphorylation, Folate Transport, and Mitochondrial Dynamics in Mouse C2C12 Myoblast Cells (2025)
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Marginal Iron Depletion Impairs Mitochondrial Complex I Activity and Reduces NDUFB8 and ISCU Protein Levels in Mouse C2C12 Myoblast Cells (2025)
Collaboration Network
Top Collaborators
- Marginal Iron Depletion Impairs Mitochondrial Complex I Activity and Reduces NDUFB8 and ISCU Protein Levels in Mouse C2C12 Myoblast Cells
- Loss of SHMT2 and Folate Deficiency Impair Protein Levels Involved in Oxidative Phosphorylation, Folate Transport, and Mitochondrial Dynamics in Mouse C2C12 Myoblast Cells
- Marginal Iron Depletion Impairs Mitochondrial Complex I Activity and Reduces NDUFB8 and ISCU Protein Levels in Mouse C2C12 Myoblast Cells
- Loss of SHMT2 and Folate Deficiency Impair Protein Levels Involved in Oxidative Phosphorylation, Folate Transport, and Mitochondrial Dynamics in Mouse C2C12 Myoblast Cells
- Marginal Iron Depletion Impairs Mitochondrial Complex I Activity and Reduces NDUFB8 and ISCU Protein Levels in Mouse C2C12 Myoblast Cells
- Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver
- Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver
- Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver
- Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver
- Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver
- Perfluorooctane sulfonic acid (PFOS) perturbs skeletal muscle oxidative phosphorylation by a different mechanism than liver
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