A
Amy Y. Sato
Assistant Professor
faculty
Physiology & Cell Biology, College of Medicine
14 h-index
43 pubs
1,183 cited
Research Areas
Links
Biography and Research Information
OverviewAI-generated summary
Amy Y. Sato is an Assistant Professor in the Department of Physiology & Cell Biology at the University of Arkansas for Medical Sciences. Her research focuses on bone metabolism and the impact of various therapeutic interventions on bone health, particularly in the context of metabolic disorders and drug-induced bone loss. Dr. Sato has investigated the effects of anabolic therapies on reversing diabetic bone signatures in mice and explored the potential of novel bone-targeted inhibitors, such as BT-Amide, for preventing glucocorticoid-induced bone loss.
Her work also delves into the cellular mechanisms regulating bone mass and strength, including the role of autophagy regulators like Tfeb in osteoblast lineage cells and the influence of lipocalin-2 on osteocyte ferroptosis and osteoblast crosstalk. Dr. Sato's publication record includes studies on the comparative efficacy of different anabolic agents, such as abaloparatide and teriparatide, in treating type 1 diabetic mice. Her scholarship metrics include an h-index of 14, with 43 publications and 1,165 citations. She has established collaborations with several researchers at her institution, including Teresita Bellido, Nisreen Akel, Gaston Troncoso, and Betiana Perez.
Metrics
- h-index: 14
- Publications: 43
- Citations: 1,183
Selected Publications
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Osteocytic Lipocalin-2 regulates bone formation locally through iron-dependent ferroptosis and Wnt suppression (2026)
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Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (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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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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CRISPR activation of <i>Tfeb</i> , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength (2024)
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Editorial: Pathophysiology of bone and mineral metabolism (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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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)
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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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Myogenic tissue nanotransfection improves muscle torque recovery following volumetric muscle loss (2022)
Grants & Funding
- TRI KL2 Scholars award - Sato UAMS Internal Research Awards Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- Sato ASBMR 2025 Young Investigator Travel Award for Allison Abney American Society for Bone and Mineral Research Principal Investigator
- TRI KL2 Scholars award - Sato UAMS Internal Research Awards Principal Investigator
- TRI KL2 Scholars award - Ashby UAMS College of Medicine Principal Investigator
- ASBMR 2025 Young Investigator Travel Grant for Sudip Panday (Sato-Mentor) American Society for Bone and Mineral Research Principal Investigator
- Glucocorticoid-induced Atrophy in Bone and Muscle NIH Co-Investigator
Collaboration Network
Top Collaborators
Teresita Bellido
Winthrop Rockefeller Foundation
9 shared publications
In database
- 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
Meloney Cregor
Indiana University School of Medicine
7 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
- 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
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
Showing 5 of 7 shared publications
Silvia Marino
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
- 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
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
Nisreen Akel
University of Arkansas for Medical Sciences
5 shared publications
In database
- 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
Intawat Nookaew
University of Arkansas for Medical Sciences
5 shared publications
In database
- Reversal of the diabetic bone signature with anabolic therapies in mice
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- 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
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
Betiana Perez
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
Gaston Troncoso
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
Jomeeka Meeks
University of Arkansas for Medical Sciences
4 shared publications
In database
- 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
Meghan Jones
University of Arkansas for Medical Sciences (US)
3 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
Scott Stewart
University of Arkansas for Medical Sciences (US)
2 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
Scott A. Stuart
University of Arkansas for Medical Sciences
2 shared publications
In database
- Author Correction: Reversal of the diabetic bone signature with anabolic therapies in mice
- THU346 Repairing Skeletal Deterioration In Diabetes With Bone Anabolic Therapies
Bhawana Adhikari
University of Arkansas for Medical Sciences
2 shared publications
In database
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway
Marjan Boerma
University of Arkansas for Medical Sciences
2 shared publications
In database
- Pharmacologic or genetic interference with atrogene signaling protects against glucocorticoid-induced musculoskeletal and cardiac disease
- OR29-04 Vitamin D Signaling Prevents Glucocorticoid-Induced Musculoskeletal Tissue Loss And Cardiac Dysfunction By Targeting The Atrogene Pathway
Kevin McAndrews
Indiana University School of Medicine
2 shared publications
- 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
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