Madeline D. Carroll
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Also affiliated: Rutgers, The State University of New Jersey (2018); Rush University Medical Center (2022–2024); Duke University (2010–2012); Regeneron (United States) (2006); University of California, Irvine (2026); Sanofi (United States) (2006); Duke Medical Center (2008–2012); Rush University (2022–2023)
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Madeline Carroll's research focuses on understanding bone fragility and its regulation at the cellular level. Her work investigates the role of specific molecules, such as Lipocalin-2, in controlling osteocyte function and bone formation. This research explores mechanisms like ferroptosis and Wnt signaling pathways that influence bone health. Carroll also contributes to the broader medical field through her publications, which include studies on patient access to healthcare, outcomes of orthopedic surgical procedures, and the examination of health information systems for children with special healthcare needs.
Her scholarly contributions are evidenced by an h-index of 10 and 366 total citations across 29 publications. Carroll collaborates with researchers at the University of Arkansas for Medical Sciences, including Neha S. Dole and Vivek Khanal, with whom she has co-authored multiple publications. Her recent work spans topics from diet-induced bone fragility to surgical case reports, indicating a diverse yet focused research trajectory.
Metrics
- h-index: 10
- Publications: 33
- Citations: 369
Selected Publications
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Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression (2026)
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Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation (2025)
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High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function (2024)
Collaboration Network
Top Collaborators
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- Lipocalin-2 Regulates Osteocyte Ferroptosis and Osteocyte-Osteoblast Crosstalk via Wnt Signaling to Control Bone Formation
- Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
- High-fat and high-carbohydrate diets increase bone fragility through TGF-β–dependent control of osteocyte function
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