Maria Almeida
Professor
Also affiliated: University of Rome Tor Vergata (2004); Universidade Federal do Rio de Janeiro (2004); Centre National de la Recherche Scientifique (2000–2002); Inserm (2016); Eli Lilly (United States) (2004); University of Arkansas Medical Center (2020–2026); Universitair Ziekenhuis Leuven (2016); Central Arkansas Veterans Healthcare System (2004–2024); Instituto Palacios (2004); Muséum national d'Histoire naturelle (1999–2002); Evolution des Régulations Endocriniennes (2000–2002); Instituto de Ciências Biomédicas Albel Salazar (1998); Freie Universität Berlin (2004); Universidad del Valle (2004); KU Leuven (2016)
Research Areas
Biomedical Subjects
Biography and Research Information
OverviewAI-generated summary
Maria Almeida's research focuses on the physiological and pathophysiological mechanisms underlying skeletal health and disease, with a particular emphasis on the roles of sex steroids, aging, and oxidative stress. Her work investigates how cellular aging impacts bone structure and function, examining differences between cortical and cancellous bone. Almeida has received significant federal funding for her investigations into the mechanisms of decreased bone formation associated with aging, as well as for studying the antagonism of RANKL signaling by estrogen in osteoclasts. These grants, totaling over $1.2 million from the National Institutes of Health, underscore the importance of her research in understanding age-related bone loss and the hormonal regulation of bone remodeling.
Her publications explore the intricate molecular pathways involved in osteoblast and osteoclast function, including the Wnt signaling pathway, beta-catenin, and Forkhead box O (FoxO) transcription factors. Almeida's research has demonstrated how oxidative stress can interfere with these critical signaling cascades in osteoblasts, contributing to age-dependent bone diseases. She also investigates the impact of mechanical signals on bone metabolism, specifically the stimulation of Piezo1 by mechanical stimuli to promote bone anabolism. Her extensive publication record and high citation count reflect her contributions to the fields of skeletal physiology, endocrinology, and aging research. Almeida actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Charles A. O’Brien, Elena Ambrogini, Olivia Reyes‐Castro, and Hayley M. Sabol.
Metrics
- h-index: 53
- Publications: 163
- Citations: 11,869
Positions
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Professor publications 2003–2026University of Arkansas for Medical Sciences Internal Medicine ORCID
Selected Publications
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Wnt10b is required for the increase in cancellous bone caused by oxidized phospholipids blockade (2026)
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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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Targeting cellular senescence alleviates bone marrow aging (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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IRE1 signaling in osteoprogenitors augments β-catenin activity and physiologic bone accrual (2026)
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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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Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength (2025)
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Estrogens protect bone mass by inhibiting NAD + metabolism in osteoclasts (2025)
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The adverse effects of chemotherapy on bone mass are not prevented by senolytics (2025)
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Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (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)
Federal Grants 3 $1,263,659 total
Different consequences of cellular aging in cortical versus cancellous bone- Resubmission
Collaboration Network
Top Collaborators
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity
- 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
Showing 5 of 37 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 37 shared publications
- 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
- 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
Showing 5 of 31 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
- Increased Lipid Oxidation Causes Oxidative Stress, Increased Peroxisome Proliferator-activated Receptor-γ Expression, and Diminished Pro-osteogenic Wnt Signaling in the Skeleton
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
- Estrogen receptor-α signaling in osteoblast progenitors stimulates cortical bone accrual
Showing 5 of 23 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 20 shared publications
- Stimulation of Piezo1 by mechanical signals promotes bone anabolism
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Neutralization of oxidized phospholipids attenuates age‐associated bone loss in mice
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
Showing 5 of 20 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
- Endogenous glucocorticoids decrease skeletal angiogenesis, vascularity, hydration, and strength in aged mice
- 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
Showing 5 of 18 shared publications
- 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
- Glucocorticoids and Tumor Necrosis Factor α Increase Oxidative Stress and Suppress Wnt Protein Signaling in Osteoblasts
Showing 5 of 18 shared publications
- Stimulation of Piezo1 by mechanical signals promotes bone anabolism
- 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
- Old age causes de novo intracortical bone remodeling and porosity in mice
Showing 5 of 17 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
- Increased Lipid Oxidation Causes Oxidative Stress, Increased Peroxisome Proliferator-activated Receptor-γ Expression, and Diminished Pro-osteogenic Wnt Signaling in the Skeleton
- FoxO proteins restrain osteoclastogenesis and bone resorption by attenuating H2O2 accumulation
Showing 5 of 16 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 16 shared publications
- Stimulation of Piezo1 by mechanical signals promotes bone anabolism
- 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
Showing 5 of 15 shared publications
- Estrogens decrease osteoclast number by attenuating mitochondria oxidative phosphorylation and ATP production in early osteoclast precursors
- Mitochondrial Sirt3 contributes to the bone loss caused by aging or estrogen deficiency
- A decrease in NAD+ contributes to the loss of osteoprogenitors and bone mass with aging
- The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice
- Mmp13 deletion in mesenchymal cells increases bone mass and may attenuate the cortical bone loss caused by estrogen deficiency
Showing 5 of 15 shared publications
- 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
- Using proteolysis-targeting chimera technology to reduce navitoclax platelet toxicity and improve its senolytic activity
- DNA damage and senescence in osteoprogenitors expressing Osx1 may cause their decrease with age
- Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence
- Elimination of senescent osteoclast progenitors has no effect on the age‐associated loss of bone mass in mice
- Increased marrow adipogenesis does not contribute to age‐dependent appendicular bone loss in female mice
Showing 5 of 9 shared publications
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