Nisreen Akel
Researcher
Also affiliated: Central Arkansas Veterans Healthcare System (2023–2026); Orthopaedic Research (2005); Institute of Molecular Biology and Biophysics (2005); John L. McClellan Memorial Veterans Hospital (2026)
Faculty Researcher
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Nisreen Akel's research focuses on skeletal health, particularly in the context of metabolic disorders like diabetes and glucocorticoid-induced bone loss. She investigates the mechanisms underlying bone remodeling and the impact of various therapeutic interventions. Her work has explored the role of chaperone-mediated autophagy in maintaining bone mass and its association with age-related bone loss in male mice. Akel has also examined the efficacy of anabolic therapies in reversing diabetic bone signatures and the potential of specific compounds, such as sclerostin antibodies and bone-targeted inhibitors like BT-Amide, in addressing bone deterioration. Her research employs animal models, including mice, and utilizes techniques such as CRISPR interference for genetic studies. Akel has authored 42 publications, accumulating over 2,000 citations, and holds an h-index of 19. She collaborates with several researchers at the University of Arkansas for Medical Sciences, including Teresita Bellido, Amy Y. Sato, Gaston Troncoso, and Betiana Perez.
Metrics
- h-index: 19
- Publications: 43
- Citations: 2,073
Selected Publications
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DMP1-Cre expressing cells mediate the gain in bone mass and strength, but not the increase in bone remodeling, induced by ligands of the parathyroid hormone receptor (2026)
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Loss of PTH 1 receptor signaling in periodontal cells drives cementum dysfunction and molar ankylosis in mice (2026)
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Generation of BT-Amide, a Bone-Targeted Pyk2 Inhibitor, Effective <i>via</i> Oral Administration, for the Prevention of Glucocorticoid-Induced Bone Loss (2024)
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Sclerostin antibody corrects periodontal disease in type 2 diabetic mice (2024)
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Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice (2024)
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THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies (2023)
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CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system (2023)
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Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice (2023)
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Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice (2023)
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Reversal of the diabetic bone signature with anabolic therapies in mice (2023)
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Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass (2022)
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Decoding the epitranscriptional landscape from native RNA sequences (2020)
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Decoding the Epitranscriptional Landscape from Native RNA Sequences (2018)
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Sclerostin Antibody Treatment Stimulates Bone Formation to Normalize Bone Mass in Male Down Syndrome Mice (2017)
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PTHrP(12-48) Modulates the Bone Marrow Microenvironment and Suppresses Human Osteoclast Differentiation and Lifespan (2017)
Collaboration Network
Top Collaborators
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Sclerostin antibody corrects periodontal disease in type 2 diabetic mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Generation of BT-Amide, a Bone-Targeted Pyk2 Inhibitor, Effective <i>via</i> Oral Administration, for the Prevention of Glucocorticoid-Induced Bone Loss
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
Showing 5 of 6 shared publications
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Sclerostin antibody corrects periodontal disease in type 2 diabetic mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Generation of BT-Amide, a Bone-Targeted Pyk2 Inhibitor, Effective <i>via</i> Oral Administration, for the Prevention of Glucocorticoid-Induced Bone Loss
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
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