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Biography and Research Information
OverviewAI-generated summary
Nisreen Akel's research focuses on bone metabolism and its disruption in conditions such as diabetes and glucocorticoid-induced bone loss. Her work investigates therapeutic strategies to reverse or prevent skeletal deterioration. Akel has studied the role of chaperone-mediated autophagy in bone mass regulation and explored the efficacy of bone-targeted inhibitors and antibodies in preclinical models. Her publications include studies on reversing diabetic bone signatures in mice using anabolic therapies and correcting periodontal disease in type 2 diabetic mice with sclerostin antibodies. Akel also explores advanced genetic engineering techniques, comparing CRISPR interference with the Cre-loxP system for cell type specificity. She has collaborated with researchers at the University of Arkansas for Medical Sciences, including Teresita Bellido, Amy Y. Sato, Gaston Troncoso, and Betiana Perez, on multiple shared publications. Akel's scholarship metrics include an h-index of 19, with 41 total publications and over 2,000 citations.
Metrics
- h-index: 19
- Publications: 42
- Citations: 2,039
Selected Publications
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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)
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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