Stavros C. Manolagas
Distinguished Professor
Also affiliated: United States Department of Veterans Affairs (1984–1987); University of California, Los Angeles (1983); University of Arkansas Medical Center (1998–2021); Veterans Health Administration (1984–1986); University of Manchester (1979); University of California San Diego (1980–1990); Central Arkansas Veterans Healthcare System (1997–2023); VA San Diego Healthcare System (1987); Richard L. Roudebush VA Medical Center (1989–1994); Salford Royal Hospital (1979); VA Sepulveda Ambulatory Care Center (1983); Scripps Clinic (1989); John L. McClellan Memorial Veterans Hospital (1995–1999); Indiana University Indianapolis (1989–1994); Indiana University School of Medicine (1989–1994); Indiana University – Purdue University Indianapolis (1989–1994); Indiana University (1989–1994)
Internal Med, College of Medicine
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Stavros C. Manolagas' research focuses on the fundamental regulatory mechanisms governing the birth and death of bone cells, with significant implications for understanding and treating osteoporosis. His work has investigated the role of various factors, including glucocorticoids, estrogen loss, and androgens, in influencing osteoblastogenesis and osteoclast development. He has also explored the impact of matrix-embedded cells on osteoclast formation and the potential of parathyroid hormone to prevent osteoblast apoptosis and increase bone formation.
Manolagas' scholarship includes over 180 publications, with an h-index of 85 and more than 29,000 citations, indicating a substantial body of highly cited work. He has served as PI on federal grants, including funding from the NIH for research on androgens, estrogens, and bone loss in males. His collaborations within the University of Arkansas for Medical Sciences include extensive work with researchers such as Horacio Gómez-Acevedo, Michela Palmieri, Elena Ambrogini, and Teenamol E. Joseph.
Metrics
- h-index: 85
- Publications: 182
- Citations: 29,399
Positions
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Distinguished Professor of Medicine and Professor of Orthopedics 2006–presentUniversity of Arkansas for Medical Sciences Internal Medicine and Orthopedics ORCID
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Distinguished Professor 1994–presentUniversity of Arkansas for Medical Sciences Internal Med, College of Medicine Institutional directory
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Retired 1994–presentVA Medical Center ORCID
Selected Publications
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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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Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass (2025)
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Plasma levels of anti phosphocholine IgM antibodies are negatively correlated with bone mineral density in humans (2025)
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OR27-02 The Bone Anabolic Effect Of An Antibody Blocking Oxidized Phospholipids Is Associated With An Increase In Wnt10b In Osteoblasts. (2023)
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RANK ligand converts the NCoR/HDAC3 co-repressor to a PGC1β- and RNA-dependent co-activator of osteoclast gene expression (2023)
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Retraction notice to “Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass” [Bone 170(2023) 116702] (2023)
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RETRACTED: Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass (2023)
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Deletion of the Scavenger Receptor Scarb1 in Myeloid Cells Does Not Affect Bone Mass (2022)
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Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency (2022)
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Mmp13 deletion in mesenchymal cells increases bone mass and attenuates the cortical bone loss caused by estrogen deficiency (2022)
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Deletion of the scavenger receptor Scarb1 in osteoblast progenitors does not affect bone mass (2022)
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Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice (2021)
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<i>Mmp-13</i> deletion in cells of the mesenchymal lineage increases bone mass, decreases endocortical osteoclast number, and attenuates the cortical bone loss caused by estrogen deficiency in mice (2021)
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Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency (2021)
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Increased marrow adipogenesis does not contribute to age‐dependent appendicular bone loss in female mice (2020)
Federal Grants 1
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Role of FoxOs in Skeletal Homeostasis- Resubmission - Continuation-Continuation - Continuation - Continuation NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Co-Investigator
- ESTROGENS AND OSTEOCLASTOGENESIS NIH Principal Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Co-Investigator
- HORMONAL CONTROL OF CYTOKINES IN BONE AND STROMAL CELLS NIH Principal Investigator
- Molecular and Cellular Mechanisms of Osteoporosis NIH Principal Investigator
- OSTEOBLAST COMMITMENT AND DIFFERENTIATION BY ANGELS NIH Co-Principal Investigator
- 1,25 DIHYDROXY VITAMIN D3 AND CELLULAR IMMUNITY NIH Principal Investigator
Collaboration Network
Top Collaborators
- Matrix-embedded cells control osteoclast formation
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Rosiglitazone Causes Bone Loss in Mice by Suppressing Osteoblast Differentiation and Bone Formation
- Divergent Effects of Selective Peroxisome Proliferator-Activated Receptor-γ2 Ligands on Adipocyte Versus Osteoblast Differentiation
Showing 5 of 57 shared publications
- Matrix-embedded cells control osteoclast formation
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Estrogens and Androgens in Skeletal Physiology and Pathophysiology
- 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
Showing 5 of 57 shared publications
- Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
- Matrix-embedded cells control osteoclast formation
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
Showing 5 of 53 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
- Wnt Proteins Prevent Apoptosis of Both Uncommitted Osteoblast Progenitors and Differentiated Osteoblasts by β-Catenin-dependent and -independent Signaling Cascades Involving Src/ERK and Phosphatidylinositol 3-Kinase/AKT
- Gone with the Wnts: β-Catenin, T-Cell Factor, Forkhead Box O, and Oxidative Stress in Age-Dependent Diseases of Bone, Lipid, and Glucose Metabolism
Showing 5 of 45 shared publications
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- 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
Showing 5 of 39 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 23 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
- Glucocorticoids and Tumor Necrosis Factor α Increase Oxidative Stress and Suppress Wnt Protein Signaling in Osteoblasts
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Increased Lipid Oxidation Causes Oxidative Stress, Increased Peroxisome Proliferator-activated Receptor-γ Expression, and Diminished Pro-osteogenic Wnt Signaling in the Skeleton
Showing 5 of 22 shared publications
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- 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
- Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss
Showing 5 of 18 shared publications
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Oxidative Stress Antagonizes Wnt Signaling in Osteoblast Precursors by Diverting β-Catenin from T Cell Factor- to Forkhead Box O-mediated Transcription
- Wnt Proteins Prevent Apoptosis of Both Uncommitted Osteoblast Progenitors and Differentiated Osteoblasts by β-Catenin-dependent and -independent Signaling Cascades Involving Src/ERK and Phosphatidylinositol 3-Kinase/AKT
- 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 17 shared publications
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- Proteasomal Degradation of Runx2 Shortens Parathyroid Hormone-induced Anti-apoptotic Signaling in Osteoblasts
- Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
Showing 5 of 16 shared publications
- Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids. Potential mechanisms of their deleterious effects on bone.
- Increased bone formation by prevention of osteoblast apoptosis with parathyroid hormone
- Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin
- Osteoblast Programmed Cell Death (Apoptosis): Modulation by Growth Factors and Cytokines
- Osteocyte Apoptosis Is Induced by Weightlessness in Mice and Precedes Osteoclast Recruitment and Bone Loss
Showing 5 of 16 shared publications
- 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
- 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
Showing 5 of 15 shared publications
- Nongenotropic, Sex-Nonspecific Signaling through the Estrogen or Androgen Receptors
- Wnt Proteins Prevent Apoptosis of Both Uncommitted Osteoblast Progenitors and Differentiated Osteoblasts by β-Catenin-dependent and -independent Signaling Cascades Involving Src/ERK and Phosphatidylinositol 3-Kinase/AKT
- Kinase-mediated regulation of common transcription factors accounts for the bone-protective effects of sex steroids
- Bisphosphonates and Estrogens Inhibit Osteocyte Apoptosis via Distinct Molecular Mechanisms Downstream of Extracellular Signal-regulated Kinase Activation
- Kinase-mediated regulation of common transcription factors accounts for the bone-protective effects of sex steroids
Showing 5 of 12 shared publications
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
- A Neutralizing Antibody Targeting Oxidized Phospholipids Promotes Bone Anabolism in Chow-Fed Young Adult Mice
- 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 11 shared publications
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
- Suppression of Autophagy in Osteocytes Mimics Skeletal Aging
- 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 10 shared publications
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