Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-08
M
Melda Onal
Federal Grant PI
Assistant Professor
Also affiliated: University of Wisconsin–Madison (2014–2019); University of Arkansas Medical Center (2011); Central Arkansas Veterans Healthcare System (2011–2016)
Physiology & Cell Biology, College of Medicine
19 h-index
37 pubs
3,267 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Melda Onal's research focuses on the cellular and molecular mechanisms of skeletal diseases, with a particular emphasis on bone metabolism and the role of autophagy. Her work investigates how cells within the bone matrix, specifically osteocytes, osteoblasts, and lining cells, contribute to osteoclast formation, a critical process in bone remodeling. Onal has explored the function of receptor activator of nuclear factor kappa-B ligand (RANKL) in this process, including its expression by B lymphocytes and its contribution to bone loss, such as that induced by ovariectomy.
Her research also examines the impact of autophagy, a cellular self-degradation process, on skeletal aging and bone mass. Studies have shown that suppression of autophagy in osteocytes can mimic skeletal aging, and that mice lacking autophagy in their osteoblast lineage exhibit low bone mass and altered osteocyte networks. Onal has received federal funding from the NIH/National Institute on Aging for her work on the role of autophagy in skeletal diseases. Additionally, she has been funded by the NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases for research on CRISPR inhibition as an alternative to Cre-loxP systems.
Her scholarship metrics include an h-index of 19, with 39 total publications and over 3,200 citations. Onal collaborates with researchers at the University of Arkansas for Medical Sciences, including Jinhu Xiong, Charles A. O’Brien, Maria Almeida, and A. Gordon James, with whom she has co-authored multiple publications.
Metrics
- h-index: 19
- Publications: 37
- Citations: 3,267
Positions
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Assistant Professor publications 2011–2026University of Arkansas for Medical Sciences Physiology & Cell Biology, College of Medicine Institutional directory
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University of Arkansas for Medical Sciences publications 2011–2026ORCID
Selected Publications
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Autophagy in Osx1-Cre-targeted cells is essential for development, growth, and maintenance of bone (2026)
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TFEB-mediated autophagy stimulation as an anabolic strategy for bone: insights from TFEB activation in the osteoblast lineage (2025)
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The Aging Landscape by scRNAseq of Mesenchymal Lineage Cells in Mouse Bone (2025)
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Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (2025)
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Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness (2025)
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A new Col1a1 conditional knock-in mouse model to study osteogenesis imperfecta (2024)
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CRISPR activation of Tfeb , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength (2024)
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Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (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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A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023)
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CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system (2023)
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Novel methods for the generation of genetically engineered animal models (2022)
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Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass (2022)
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Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo (2021)
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Effective CRISPR interference of an endogenous gene via a single transgene in mice (2019)
Federal Grants 2 $650,031 total
NIH
Contact PI
Jun 2026 - Mar 2031
NIH
Contact PI
Jan 2020 - Dec 2021
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- DEAP Awards - P. Drew - UAMS VCRI - FY26 Role of Oligodendrocyte-Lineage Cells in FASD UAMS Division of Research and Innovation Principal Investigator
Collaboration Network
Top Collaborators
Jinhu Xiong
University of Arkansas for Medical Sciences
15 shared publications
In database
- Matrix-embedded cells control osteoclast formation
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Receptor Activator of Nuclear Factor κB Ligand (RANKL) Protein Expression by B Lymphocytes Contributes to Ovariectomy-induced Bone Loss
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
Showing 5 of 15 shared publications
Charles A. O’Brien
University of Arkansas for Medical Sciences
15 shared publications
In database
- Matrix-embedded cells control osteoclast formation
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Receptor Activator of Nuclear Factor κB Ligand (RANKL) Protein Expression by B Lymphocytes Contributes to Ovariectomy-induced Bone Loss
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
Showing 5 of 15 shared publications
Maria Almeida
University of Arkansas for Medical Sciences
11 shared publications
In database
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Receptor Activator of Nuclear Factor κB Ligand (RANKL) Protein Expression by B Lymphocytes Contributes to Ovariectomy-induced Bone Loss
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
- Low bone mass and changes in the osteocyte network in mice lacking autophagy in the osteoblast lineage
- Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone
Showing 5 of 11 shared publications
Jeff D. Thostenson
University of Arkansas for Medical Sciences
8 shared publications
In database
- Receptor Activator of Nuclear Factor κB Ligand (RANKL) Protein Expression by B Lymphocytes Contributes to Ovariectomy-induced Bone Loss
- Low bone mass and changes in the osteocyte network in mice lacking autophagy in the osteoblast lineage
- A Novel Distal Enhancer Mediates Inflammation‐, PTH‐, and Early Onset Murine Kidney Disease‐Induced Expression of the Mouse Fgf23 Gene
- Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone
- Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo
Showing 5 of 8 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
7 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Effective CRISPR interference of an endogenous gene via a single transgene in mice
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- CRISPR interference provides increased cell type-specificity compared to the Cre-loxP system
- The Aging Landscape by scRNAseq of Mesenchymal Lineage Cells in Mouse Bone
Showing 5 of 7 shared publications
A. Gordon James
University of Arkansas for Medical Sciences
6 shared publications
In database
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- The Aging Landscape by scRNAseq of Mesenchymal Lineage Cells in Mouse Bone
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- Loss of chaperone‐mediated autophagy does not alter age‐related bone loss in male mice
- CRISPR activation of Tfeb , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
Showing 5 of 6 shared publications
Qiang Fu
University of Arkansas for Medical Sciences
5 shared publications
In database
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- The RANKL Distal Control Region Is Required for the Increase in RANKL Expression, But Not the Bone Loss, Associated with Hyperparathyroidism or Lactation in Adult Mice
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
Robert S. Weinstein
Central Arkansas Veterans Healthcare System (US)
5 shared publications
- Matrix-embedded cells control osteoclast formation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
- Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone
- The RANKL Distal Control Region Is Required for the Increase in RANKL Expression, But Not the Bone Loss, Associated with Hyperparathyroidism or Lactation in Adult Mice
Stavros C. Manolagas
Central Arkansas Veterans Healthcare System
5 shared publications
In database
- Matrix-embedded cells control osteoclast formation
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Receptor Activator of Nuclear Factor κB Ligand (RANKL) Protein Expression by B Lymphocytes Contributes to Ovariectomy-induced Bone Loss
- Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone
- The RANKL Distal Control Region Is Required for the Increase in RANKL Expression, But Not the Bone Loss, Associated with Hyperparathyroidism or Lactation in Adult Mice
Julie Crawford
Institute for Musculoskeletal Health
5 shared publications
In database
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- 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
- CRISPR activation of Tfeb , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
M. Piemontese
Central Arkansas Veterans Healthcare System (US)
4 shared publications
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
- Low bone mass and changes in the osteocyte network in mice lacking autophagy in the osteoblast lineage
- Suppression of autophagy in osteocytes does not modify the adverse effects of glucocorticoids on cortical bone
James A. Hendrixson
University of Arkansas for Medical Sciences
4 shared publications
In database
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- 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
- CRISPR activation of Tfeb , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
Ilham Kadhim
University of Arkansas for Medical Sciences
4 shared publications
In database
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness
- CRISPR activation of Tfeb , a master regulator of autophagy and lysosomal biogenesis, in osteoblast lineage cells increases bone mass and strength
- Autophagy in Osx1-Cre-targeted cells is essential for development, growth, and maintenance of bone
Robert L. Jilka
Central Arkansas Veterans Healthcare System
3 shared publications
In database
- Matrix-embedded cells control osteoclast formation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
Ryan S. MacLeod
University of Arkansas for Medical Sciences (US)
3 shared publications
- Effective CRISPR interference of an endogenous gene via a single transgene in mice
- Loss of chaperone-mediated autophagy is associated with low vertebral cancellous bone mass
- Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo
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