Teresita Bellido
Sourced from institutional research profiles (UAMS TRI or ARA).
Musculoskeletal Health and Disease Research - UAMS Creativity Hub Leadership
Also affiliated: Indiana University Health (2020–2026); United States Department of Veterans Affairs (1993–2016); University of Indianapolis (2014–2019); University of Arkansas Medical Center (1998); Central Arkansas Veterans Healthcare System (2001–2026); Richard L. Roudebush VA Medical Center (1993–2024); Geriatric Research Education and Clinical Center (1997); Winthrop Rockefeller Foundation (2021–2026); Bone Health and Osteoporosis Foundation (2007); Juliana Kinderziekenhuis (2016–2018); University School (2013–2019); John L. McClellan Memorial Veterans Hospital (2021–2024); Institute of Cell Biology and Neurobiology (1987–2015); Larue Carter Hospital (1993); Indiana Hemophilia and Thrombosis Center (2017–2022); Indiana University Indianapolis (2016–2019); Indiana University School of Medicine (1994–2024); Indiana University – Purdue University Indianapolis (1993–2026); Universidad Nacional del Sur (1987–2009); Indiana University (2011–2020)
Faculty Researcher
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Teresita Bellido's research focuses on the cellular and molecular mechanisms underlying bone and musculoskeletal diseases. Her work investigates the role of osteocytes as signaling cells and their contribution to conditions such as diabetes-induced bone disease and multiple myeloma. Bellido has received federal funding for several projects, including a $331,057 NIH/NIAMS grant to study glucocorticoid-induced atrophy in bone and muscle, and a $454,799 NIH/NCI grant as Co-PI to examine the contribution of osteocytes to the musculoskeletal effects of multiple myeloma. She also received funding from the NSF for workshops on musculoskeletal biology.
Her publications include studies on the osteocyte's function in signaling, the use of decellularized matrices to accelerate bone repair, and the impact of Notch signaling in the bone marrow niche on tumor growth and bone destruction. Bellido's research also extends to the reversal of diabetic bone signatures with anabolic therapies and the mechanisms of PTH receptor signaling in diabetes-induced bone disease. She has a distinguished publication record, with an h-index of 75 and over 23,000 citations across nearly 300 publications. Bellido leads an active research group at the University of Arkansas for Medical Sciences and collaborates with several researchers within the institution.
Metrics
- h-index: 75
- Publications: 294
- Citations: 23,223
Selected Publications
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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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Region- and Compartment-Specific Elevation of Bone Mass in Mice Following Tsc1 Deletion in 8-kb Dmp1-Cre-Expressing Cells (2026)
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Upregulation of Parathyroid Hormone Receptor 1 (PTH1R) in Non-Mechanostimulated Osteocytes Under High-Glucose Conditions Promotes a Macrophage Pro-Inflammatory and Osteoclastogenic Phenotype via IL-6 Secretion (2026)
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Osteocytes Produces RANKL Via Wnt-TGFβ Signaling Axis for Osteoclastogenesis (2025)
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Caveolin‐1 Regulates Parathyroid Hormone (PTH)‐Related Protein (PTHrP) Actions on PTH Receptor Type 1 in Bone Cells (2025)
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The development of a collagen-nanoscale hydroxyapatite three-dimensional (3D) in vitro culture system for reproducing osteocyte differentiation and tissue mineralization (2025)
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A novel CCL3-HMGB1 signaling axis regulating osteocyte RANKL expression in multiple myeloma (2024)
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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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Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease (2024)
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Sclerostin antibody corrects periodontal disease in type 2 diabetic mice (2024)
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PTH receptor signalling, osteocytes and bone disease induced by diabetes mellitus (2024)
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Abaloparatide is more potent than teriparatide in restoring bone mass and strength in type 1 diabetic male mice (2024)
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Proceedings of the 2023 Santa Fe Bone Symposium: Progress and Controversies in the Management of Patients with Skeletal Diseases (2023)
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OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway (2023)
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THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies (2023)
ARA Academy 2018 ARA Scholar
Dr. Bellido is an internationally recognized leader in bone research. She holds major grants from the NIH and Veterans Administration and has served as president of the American Society for Bone and Mineral Research (2020). Her research focuses on signal transduction in bone and muscle, with emphasis on osteocyte biology in health and disease and hormonal action mechanisms in the musculoskeletal system.
Policy Impact
Holds major NIH and VA grants; former president of the American Society for Bone and Mineral Research, bringing national leadership and federal funding to UAMS.
Growth Areas
['Population Health Innovations & Clinical Research']
Federal Grants 7 $805,856 total
BCCMA: Foundational Research to Act Upon and Resist Conditions Unfavorable to Bone (FRACTURE CURB)
Contribution of osteocytes to the musculoskeletal effects of Multiple Myeloma
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- PPARG regulates osteocyte function during aging NIH/Nat. Inst. on Aging via University of Toledo
- ASBMR Three Year Pre-Meeting Symposia NIH
- CYTOKINE SIGNAL TRANSDUCTION IN OSTEOBLASTIC CELLS NIH
- Cytokine Signal Transduction in Osteoblastic Cells NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases
- Osteocyte control of bone formation via Sost NIH
- 2022 Musculoskeletal Biology Workshop National Science Foundation
- Bisphosphonate binding to connexin43-expressing cells NIH
- 2023 Orthopedic Research Society Musculoskeletal Biology Workshop National Science Foundation
- Eighteenth Forum on Osteoporosis and Metabolic Bone Diseases for Fellows in Training NIH
Collaboration Network
Top Collaborators
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Abaloparatide is more potent than teriparatide in restoring bone mass and strength in type 1 diabetic male mice
Showing 5 of 11 shared publications
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Myogenic tissue nanotransfection improves muscle torque recovery following volumetric muscle loss
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Abaloparatide is more potent than teriparatide in restoring bone mass and strength in type 1 diabetic male mice
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
Showing 5 of 9 shared publications
- The osteocyte as a signaling cell
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- A novel CCL3-HMGB1 signaling axis regulating osteocyte RANKL expression in multiple myeloma
- Wnt/β-catenin Signaling Controls Maxillofacial Hyperostosis
Showing 5 of 7 shared publications
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- Abstract 5672: Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- 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
- Abaloparatide is more potent than teriparatide in restoring bone mass and strength in type 1 diabetic male mice
- 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
- 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
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- A novel CCL3-HMGB1 signaling axis regulating osteocyte RANKL expression in multiple myeloma
- Abstract 5672: Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Data from Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Abstract 5672: Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Data from Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Abaloparatide is more potent than teriparatide in restoring bone mass and strength in type 1 diabetic male mice
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- Data from Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Abstract 5672: Notch3 signaling between myeloma cells and osteocytes in the tumor niche promotes tumor growth and bone destruction
- Data from Targeting Notch Inhibitors to the Myeloma Bone Marrow Niche Decreases Tumor Growth and Bone Destruction without Gut Toxicity
- Wnt/β-catenin Signaling Controls Maxillofacial Hyperostosis
- Sclerostin antibody corrects periodontal disease in type 2 diabetic mice
- Type 1 diabetes mellitus leads to gingivitis and an early compensatory increase in bone remodeling
- The <scp>LRP5</scp> high‐bone‐mass mutation causes alveolar bone accrual with minor craniofacial alteration
- 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
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