J
Joanna Fiddler Data-verified
Affiliation confirmed via AI analysis of OpenAlex, ORCID, and web sources.
Assistant Professor
faculty
6 h-index
31 pubs
113 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Joanna Fiddler's research investigates the role of mitochondria in cellular metabolism and the impact of nutrient deficiencies and pharmacological agents on mitochondrial function. Her work has explored how reduced expression of enzymes like SHMT2 (serine hydroxymethyltransferase 2) affects mitochondrial folate accumulation, respiration, and leads to uracil accumulation in mitochondrial DNA, as observed in mouse models. Fiddler has also examined the influence of vitamin B12 status and folic acid supplementation on mitochondrial heteroplasmy levels in mice. Her research extends to the cardiac effects of selective serotonin reuptake inhibitors (SSRIs), identifying mitochondrial and sarcomere dysfunction as mechanisms of SSRI-induced cardiotoxicity. Additionally, her investigations include the metabolic responses of C2C12 myoblast cells to iron depletion and the evaluation of reference genes for gene expression analysis in animal models of dietary deficiencies. Fiddler's publication record includes studies on ferritin measurement in whole blood and the energy metabolism of myoblasts under varying substrate availability.
Metrics
- h-index: 6
- Publications: 31
- Citations: 113
Selected Publications
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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
Martha S. Field
Cornell University (US)
12 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Vitamin B12 status and folic acid supplementation influence mitochondrial heteroplasmy levels in mice
- Impairments in SHMT2 expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
Showing 5 of 12 shared publications
Jamie Blum
Cornell University (US)
6 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Impairments in SHMT2 expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
- Loss of SHMT2 and Folate Deficiency Impair Energy Metabolism in Mouse Embryonic Fibroblasts Cells
- Impairments in <i>SHMT2</i> expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
Showing 5 of 6 shared publications
Anna Thalacker‐Mercer
University of Alabama at Birmingham (US)
6 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Impairments in SHMT2 expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
- Loss of SHMT2 and Folate Deficiency Impair Energy Metabolism in Mouse Embryonic Fibroblasts Cells
- Impairments in <i>SHMT2</i> expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
Showing 5 of 6 shared publications
Yuwen Xiu
Cornell University (US)
4 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
- Reduced methionine synthase ( <i>Mtr</i> ) expression creates a functional vitamin B12 deficiency that leads to uracil accumulation in mouse mitochondrial DNA
Whitney N. Phinney
University of Colorado Denver (US)
4 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
- Reduced methionine synthase ( <i>Mtr</i> ) expression creates a functional vitamin B12 deficiency that leads to uracil accumulation in mouse mitochondrial DNA
Katarina E. Heyden
4 shared publications
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Impairments in SHMT2 expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
- Reduced methionine synthase ( <i>Mtr</i> ) expression creates a functional vitamin B12 deficiency that leads to uracil accumulation in mouse mitochondrial DNA
- P30-016-23 Disruption of Mitochondrial Folate Metabolism Leads to Mitochondrial DNA Leakage and Apoptosis
Sally P. Stabler
University of Colorado Denver (US)
3 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
Abigail L Zirbel
University of Arkansas at Fayetteville (US)
3 shared publications
- Energy Metabolism in C2C12 Myoblast Cells Exposed to Marginal to Severe Iron Depletion Is Influenced by Substrate Availability
- 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
Makenzie A Tharpe
University of Arkansas at Fayetteville (US)
3 shared publications
- Energy Metabolism in C2C12 Myoblast Cells Exposed to Marginal to Severe Iron Depletion Is Influenced by Substrate Availability
- 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
Simon G. Lamarre
Université de Moncton (CA)
2 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
Margaret E. Brosnan
Memorial University of Newfoundland (CA)
2 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
John T. Brosnan
Memorial University of Newfoundland (CA)
2 shared publications
- Reduced Shmt2 Expression Impairs Mitochondrial Folate Accumulation and Respiration, and Leads to Uracil Accumulation in Mouse Mitochondrial DNA
- Reduced <i>Shmt2</i> expression impairs mitochondrial folate accumulation and respiration, and leads to uracil accumulation in mouse mitochondrial DNA
Luisa F. Castillo
Cornell University (US)
2 shared publications
- Impairments in SHMT2 expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
- Impairments in <i>SHMT2</i> expression or cellular folate availability reduce oxidative phosphorylation and pyruvate kinase activity
Olga Malysheva
Cornell University (US)
2 shared publications
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Reduced methionine synthase ( <i>Mtr</i> ) expression creates a functional vitamin B12 deficiency that leads to uracil accumulation in mouse mitochondrial DNA
Michal K. Handzlik
La Jolla Bioengineering Institute (US)
2 shared publications
- Reduced methionine synthase expression results in uracil accumulation in mitochondrial DNA and impaired oxidative capacity
- Reduced methionine synthase ( <i>Mtr</i> ) expression creates a functional vitamin B12 deficiency that leads to uracil accumulation in mouse mitochondrial DNA
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