Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Vivek Khanal's research focuses on the impact of diet on bone health and the underlying molecular mechanisms. His work investigates how high-fat and high-carbohydrate diets can increase bone fragility, identifying the transforming growth factor-beta (TGF-β) signaling pathway as a key regulator of osteocyte function in this process. Khanal also studies the role of lipocalin-2 in osteocytes, exploring its regulation of bone formation through ferroptosis and Wnt signaling pathways. His research extends to autophagy's essential role in bone development, growth, and maintenance. Additionally, Khanal examines global transcriptional profiles of adipose tissue to uncover sex-dependent mechanisms in acute obesity and their implications for interorgan crosstalk. His collaborators at the University of Arkansas for Medical Sciences include Neha S. Dole, Madeline Carroll, Amy Y. Sato, and Ryan M. Allen.
Metrics
- h-index: 2
- Publications: 5
- Citations: 21
Positions
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Postdoctoral Fellow publications 2024–2026University of Arkansas for Medical Sciences Institution web page
Selected Publications
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Autophagy in Osx1-Cre-targeted cells is essential for development, growth, and maintenance of bone (2026)
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Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression (2026)
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Global Transcriptional Profiling of Adipose Tissue Uncovers Unique Sex-Dependent Mechanisms in Acute Obesity: Implications for Adipose-Heart Interorgan Crosstalk (2025)
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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
- Global Transcriptional Profiling of Adipose Tissue Uncovers Unique Sex-Dependent Mechanisms in Acute Obesity: Implications for Adipose-Heart Interorgan Crosstalk
- Autophagy in Osx1-Cre-targeted cells is essential for development, growth, and maintenance of bone
- 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
- 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
- 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
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