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Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-06
N
Nisreen S. Akel
Research Associate
Also affiliated: Kurume University (2008); University of Arkansas Medical Center (2017); Central Arkansas Veterans Healthcare System (2023–2026); John L. McClellan Memorial Veterans Hospital (2023–2026)
19 h-index
43 pubs
2,085 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Nisreen S. Akel's research has focused on bone metabolism and the mechanisms underlying bone diseases. Her work has investigated the role of specific molecules, such as Interleukin-8 (IL-8), in stimulating osteoclastogenesis and bone resorption, particularly in the context of metastatic bone disease and breast cancer bone metastasis. Akel has also explored other factors influencing bone mass and strength, including inhibin A and platelet-derived factors in murine models. Her publications also touch upon the skeletal response to disuse in aging rats and bone density in individuals with Down syndrome. Akel has a scholarship h-index of 19, with 43 total publications and over 2,000 citations. She has collaborated extensively with 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: 2,085
Positions
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Research Associate publications 2003–2026University of Arkansas for Medical Sciences Institution web page
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 via 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
Dana Gaddy
University of Arkansas for Medical Sciences (US)
18 shared publications
- Interleukin-8 stimulation of osteoclastogenesis and bone resorption is a mechanism for the increased osteolysis of metastatic bone disease
- Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
- Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
- Low bone turnover and low bone density in a cohort of adults with Down syndrome
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
Showing 5 of 18 shared publications
Larry J. Suva
University of Arkansas for Medical Sciences (US)
15 shared publications
- Interleukin-8 stimulation of osteoclastogenesis and bone resorption is a mechanism for the increased osteolysis of metastatic bone disease
- Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
- Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
- Low bone turnover and low bone density in a cohort of adults with Down syndrome
- Platelet Dysfunction and a High Bone Mass Phenotype in a Murine Model of Platelet-Type von Willebrand Disease
Showing 5 of 15 shared publications
Teresita Bellido
Central Arkansas Veterans Healthcare System
8 shared publications
In database
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Sclerostin antibody corrects periodontal disease in type 2 diabetic mice
- Generation of BT-Amide, a Bone-Targeted Pyk2 Inhibitor, Effective via Oral Administration, for the Prevention of Glucocorticoid-Induced Bone Loss
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Loss of PTH 1 receptor signaling in periodontal cells drives cementum dysfunction and molar ankylosis in mice
Showing 5 of 8 shared publications
Frances L. Swain
University of Arkansas for Medical Sciences (US)
7 shared publications
- Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
- Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
- Low Bone Turnover and Low BMD in Down Syndrome: Effect of Intermittent PTH Treatment
- Sc65 Is a Novel Endoplasmic Reticulum Protein That Regulates Bone Mass Homeostasis
Showing 5 of 7 shared publications
Robert A. Skinner
Institute of Molecular Biology and Biophysics (RU)
7 shared publications
- Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
- Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
- Platelet Dysfunction and a High Bone Mass Phenotype in a Murine Model of Platelet-Type von Willebrand Disease
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
- Low Bone Turnover and Low BMD in Down Syndrome: Effect of Intermittent PTH Treatment
Showing 5 of 7 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
7 shared publications
In database
- Decoding the epitranscriptional landscape from native RNA sequences
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Decoding the Epitranscriptional Landscape from Native RNA Sequences
- 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
Showing 5 of 7 shared publications
Maxim Dobretsov
University of Arkansas for Medical Sciences (US)
5 shared publications
- Degenerative Tissue Responses to Space-like Radiation Doses in a Rodent Model of Simulated Microgravity.
- PANCREATIC HISTOLOGY AND ASSOCIATED BIOCHEMICAL CHANGES IN RATS ON HIND-LIMB SUSPENSION
- Animal Model of Simulated Microgravity: A comparative study of hindlimb unloading via tail vs. pelvic suspension
- Radiation combined with hind‐limb suspension affects physiological parameters in rats (1103.7)
- X‐irradiation and Simulated Microgravity affects Rat Weight, Food Intake, Insulin and Paw Pressure Pain Threshold
Silvia Marino
University of Arkansas for Medical Sciences (US)
5 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
Shenyang Li
Central Arkansas Veterans Healthcare System (US)
5 shared publications
- 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
- 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
Amy Y. Sato
University of Arkansas for Medical Sciences
5 shared publications
In database
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Generation of BT-Amide, a Bone-Targeted Pyk2 Inhibitor, Effective via Oral Administration, for the Prevention of Glucocorticoid-Induced Bone Loss
- 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
Tristan W. Fowler
University of Arkansas for Medical Sciences (US)
4 shared publications
- Low bone turnover and low bone density in a cohort of adults with Down syndrome
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
- Low Bone Turnover and Low BMD in Down Syndrome: Effect of Intermittent PTH Treatment
- Activin A inhibits RANKL-mediated osteoclast formation, movement and function in murine bone marrow macrophage cultures
Manali Bendre
Orthopaedic Research (GB)
4 shared publications
- Interleukin-8 stimulation of osteoclastogenesis and bone resorption is a mechanism for the increased osteolysis of metastatic bone disease
- Tumor-Derived Interleukin-8 Stimulates Osteolysis Independent of the Receptor Activator of Nuclear Factor-κB Ligand Pathway
- Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
William R. Hogue
University of Arkansas for Medical Sciences (US)
4 shared publications
- Inhibin A Is an Endocrine Stimulator of Bone Mass and Strength
- Platelet Dysfunction and a High Bone Mass Phenotype in a Murine Model of Platelet-Type von Willebrand Disease
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
- Low Bone Turnover and Low BMD in Down Syndrome: Effect of Intermittent PTH Treatment
Archana Kamalakar
University of Arkansas for Medical Sciences (US)
4 shared publications
- Circulating interleukin-8 levels explain breast cancer osteolysis in mice and humans
- Activin A inhibits RANKL-mediated osteoclast formation, movement and function in murine bone marrow macrophage cultures
- PTHrP(12-48) Modulates the Bone Marrow Microenvironment and Suppresses Human Osteoclast Differentiation and Lifespan
- Abstract 1041: PTHrP(12-48) localization is intracellular and it inhibits cell proliferation and osteoclastogenesis
Meloney Cregor
University of Arkansas for Medical Sciences (US)
4 shared publications
- 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
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