Charles A. O’Brien
Professor of Medicine
Also affiliated: United States Department of Veterans Affairs (1989); Inserm (2016); University of Arkansas Medical Center (2000–2024); Universitair Ziekenhuis Leuven (2016); Oklahoma Medical Research Foundation (1989–1995); Yale University (1993–1994); Central Arkansas Veterans Healthcare System (2001–2026); Oklahoma City VA Medical Center (1989); Bone Health and Osteoporosis Foundation (2016); University of Oklahoma Health Sciences Center (1989–1990); Centers for Medicare and Medicaid Services (1995); University of Oklahoma (1990–1995); The University of Texas Health Science Center at Houston (1989); KU Leuven (2016)
Internal Med, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Charles A. O’Brien is a Professor of Medicine at the University of Arkansas for Medical Sciences, with a research focus on bone metabolism and the cellular and molecular mechanisms underlying skeletal health and disease. His work investigates the roles of hormones, oxidative stress, and cellular aging in bone remodeling and involution. O’Brien has been awarded five federal grants totaling $2,988,579, including significant funding from the National Institutes of Health (NIH) for projects such as the Center for Musculoskeletal Disease Research (CMDR) and research into osteocyte control of bone remodeling. He has also received funding for studies on the molecular mechanisms of glucocorticoid-induced bone loss and bone loss in osteomyelitis.
His scholarship metrics include an h-index of 64, with over 18,000 citations across 189 publications, identifying him as a highly cited researcher. O’Brien’s publications address topics including the control of osteoclast formation by matrix-embedded cells, the signaling pathways of sex steroid receptors in skeletal physiology, and the impact of oxidative stress and chronic parathyroid hormone elevation on bone. He has a notable collaborative network, with numerous shared publications with colleagues at the University of Arkansas for Medical Sciences, including Elena Ambrogini, Olivia Reyes‐Castro, Maria Almeida, and Hayley M. Sabol.
O’Brien's research also examines the direct effects of glucocorticoids on osteoblasts and osteocytes, leading to apoptosis and reduced bone formation and strength. Further investigations explore how skeletal involution is influenced by age-associated oxidative stress and the loss of sex steroids, and how Wnt signaling in osteoblast precursors is affected by oxidative stress. His ongoing work contributes to a broader understanding of bone diseases and potential therapeutic targets.
Metrics
- h-index: 64
- Publications: 187
- Citations: 18,048
Positions
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Professor of Medicine 1994–presentUniversity of Arkansas for Medical Sciences Internal Med, College of Medicine Institutional directory
Selected Publications
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Protocol for the enrichment of endosteal and periosteal mesenchymal cells from murine bone for single-cell transcriptome analysis (2026)
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A transcriptomic-driven segmentation and cell simulation framework for high-resolution spatial transcriptomics and cell-cell communication (2026)
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Mechanistic insights into the pathogenesis and therapeutic recalcitrance of Staphylococcus aureus osteomyelitis (2026)
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Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass (2025)
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The Aging Landscape by scRNAseq of Mesenchymal Lineage Cells in Mouse Bone (2025)
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Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
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Potent suppression of bone remodeling by denosumab does not blunt the anabolic response to romosozumab in mice (2025)
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Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025)
Federal Grants 5 $2,988,579 total
Different consequences of cellular aging in cortical versus cancellous bone- Resubmission
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Center for Musculoskeletal Disease Research (COBRE) NIH/Nat. Inst. of General Medical Sciences Principal Investigator
- In Vivo Regulation of IL6 and IL6R Gene Expression NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
- ABI C. OBrien NIH COBRE FY26 Y4 State of Arkansas Principal Investigator
- RANKL and Lymphocyte Mediated Bone Loss Veterans Administration Principal Investigator
- Center for Studies of Host Response to Cancer Therapy NIH Co-Investigator
- IN VIVO REGULATION OF IL6 AND IL6R GENE EXPRESSION NIH Principal Investigator
- Molecular and Cellular Mechanisms of Osteoporosis NIH Co-Investigator
- A Transgenic Rat for Noninvasive Assessment of Chondrogenic Activity in vivo NIH Co-Investigator
- Different consequences of cellular aging in cortical versus cancellous bone NIH/Nat. Inst. on Aging Co-Principal Investigator
Collaboration Network
Top Collaborators
- Matrix-embedded cells control osteoclast formation
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Glucocorticoids Act Directly on Osteoblasts and Osteocytes to Induce Their Apoptosis and Reduce Bone Formation and Strength
- Chronic Elevation of Parathyroid Hormone in Mice Reduces Expression of Sclerostin by Osteocytes: A Novel Mechanism for Hormonal Control of Osteoblastogenesis
- Oxidative Stress Antagonizes Wnt Signaling in Osteoblast Precursors by Diverting β-Catenin from T Cell Factor- to Forkhead Box O-mediated Transcription
Showing 5 of 38 shared publications
- Estrogens and Androgens in Skeletal Physiology and Pathophysiology
- The role of estrogen and androgen receptors in bone health and disease
- Oxidative Stress Antagonizes Wnt Signaling in Osteoblast Precursors by Diverting β-Catenin from T Cell Factor- to Forkhead Box O-mediated Transcription
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
Showing 5 of 35 shared publications
- Matrix-embedded cells control osteoclast formation
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Glucocorticoids Act Directly on Osteoblasts and Osteocytes to Induce Their Apoptosis and Reduce Bone Formation and Strength
- Glucocorticoids Act Directly on Osteoclasts to Increase Their Life Span and Reduce Bone Density
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
Showing 5 of 29 shared publications
- Matrix-embedded cells control osteoclast formation
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
Showing 5 of 25 shared publications
- 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
- Osteocyte RANKL: New insights into the control of bone remodeling
- 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
Showing 5 of 24 shared publications
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Old age causes de novo intracortical bone remodeling and porosity in mice
- DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age
- Sirtuin1 (Sirt1) Promotes Cortical Bone Formation by Preventing β-Catenin Sequestration by FoxO Transcription Factors in Osteoblast Progenitors
- The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct
Showing 5 of 19 shared publications
- Estrogens and Androgens in Skeletal Physiology and Pathophysiology
- The role of estrogen and androgen receptors in bone health and disease
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
Showing 5 of 19 shared publications
- 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 16 shared publications
- Receptor Activator of Nuclear Factor κB Ligand (RANKL) Protein Expression by B Lymphocytes Contributes to Ovariectomy-induced Bone Loss
- Old age causes de novo intracortical bone remodeling and porosity in mice
- Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency
- Low bone mass and changes in the osteocyte network in mice lacking autophagy in the osteoblast lineage
- The Effects of Aging and Sex Steroid Deficiency on the Murine Skeleton Are Independent and Mechanistically Distinct
Showing 5 of 16 shared publications
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- The Estrogen Receptor-α in Osteoclasts Mediates the Protective Effects of Estrogens on Cancellous But Not Cortical Bone
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- FOXOs attenuate bone formation by suppressing Wnt signaling
Showing 5 of 15 shared publications
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- 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
- Single-Cell Transcriptomic Analysis Identifies Senescent Osteocytes That Trigger Bone Destruction in Breast Cancer Metastasis
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
Showing 5 of 14 shared publications
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- FoxO-Mediated Defense against Oxidative Stress in Osteoblasts Is Indispensable for Skeletal Homeostasis in Mice
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
Showing 5 of 13 shared publications
- Chronic Elevation of Parathyroid Hormone in Mice Reduces Expression of Sclerostin by Osteocytes: A Novel Mechanism for Hormonal Control of Osteoblastogenesis
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
- Parathyroid Hormone Controls Receptor Activator of NF-κB Ligand Gene Expression via a Distant Transcriptional Enhancer
- Targeted Deletion of a Distant Transcriptional Enhancer of the Receptor Activator of Nuclear Factor-κB Ligand Gene Reduces Bone Remodeling and Increases Bone Mass
- IL-6 is not required for parathyroid hormone stimulation of RANKL expression, osteoclast formation, and bone loss in mice
Showing 5 of 13 shared publications
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Glucocorticoids Act Directly on Osteoblasts and Osteocytes to Induce Their Apoptosis and Reduce Bone Formation and Strength
- Chronic Elevation of Parathyroid Hormone in Mice Reduces Expression of Sclerostin by Osteocytes: A Novel Mechanism for Hormonal Control of Osteoblastogenesis
- Control of Bone Mass and Remodeling by PTH Receptor Signaling in Osteocytes
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
Showing 5 of 12 shared publications
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Reduced osteoprotegerin expression by osteocytes may contribute to rebound resorption after denosumab discontinuation
- Single-cell Transcriptome Analysis Identifies Senescent Osteocytes as Contributors to Bone Destruction in Breast Cancer Metastasis
- Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass
- RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass
Showing 5 of 10 shared publications
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