Match tier
Listed
Presence
Current · Arkansas
Last published
2026
Sources
OpenAlex · ORCID
Refreshed
2026-10-09
J
Jinhu Xiong
Federal Grant PI
High Impact
Associate Professor
Also affiliated: University of Arkansas Medical Center (2011–2025); Central Arkansas Veterans Healthcare System (2011–2018); Bone Health and Osteoporosis Foundation (2016)
Orthopaedics Surgery, College of Medicine
22 h-index
41 pubs
4,480 cited
Research Areas
Biomedical Subjects
Links
Biography and Research Information
OverviewAI-generated summary
Jinhu Xiong, an Associate Professor in Orthopaedic Surgery at the University of Arkansas for Medical Sciences, investigates the cellular mechanisms regulating bone remodeling and aging. His research focuses on the roles of osteocytes, osteoblasts, and osteoclasts in bone homeostasis, particularly in the context of aging mice. Xiong has received funding from the National Institutes of Health for his work on Piezo1's role in bone mechanotransduction and homeostasis.
His publications detail how matrix-embedded cells, specifically osteocytes, are a primary source of RANKL that drives osteoclast formation. Additional research explores how suppression of autophagy in osteocytes can mimic skeletal aging and how estrogen receptor-alpha signaling influences bone accrual. Xiong's scholarship metrics include an h-index of 22 with over 4,400 citations across 42 publications. He actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Melda Onal, Charles A. O’Brien, Maria Almeida, and Ha‐Neui Kim.
Metrics
- h-index: 22
- Publications: 41
- Citations: 4,480
Positions
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Associate Professor publications 2011–2026University of Arkansas for Medical Sciences Orthopaedics Surgery, College of Medicine Institutional directory
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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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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Dissecting primary versus secondary effects of osteogenesis imperfecta on abnormal lung development and function (2026)
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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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Different effects of moderate tibial loading and Yoda1 on breast cancer-induced osteolysis in aged mice (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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Piezo1 expression in mature osteocytes is dispensable for the skeletal response to mechanical loading (2024)
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Mitigating aging and doxorubicin induced bone loss in mature mice via mechanobiology based treatments (2024)
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Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (2024)
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A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023)
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Piezo1 opposes age‐associated cortical bone loss (2023)
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Piezo1 stimulates mitochondrial function via cAMP signaling (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)
Federal Grants 1 $464,150 total
NIH
Contact PI
Aug 2020 - Jul 2031
The role of Piezo1 in bone homeostasis and mechanotransduction
Grants & Funding
As listed on this researcher's institutional profile. Federal awards with verified records are shown above.
- Osteocyte Control of Bone Remodeling NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Co-Investigator
- Center for Musculoskeletal Disease Research (CMDR) NIH/Nat. Inst. of General Medical Sciences Co-Investigator
- The role of Piezo 1 in bone homeostasis and mechanotransduction NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
Collaboration Network
Top Collaborators
Charles A. O’Brien
University of Arkansas for Medical Sciences
24 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
- 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
Melda Onal
University of Arkansas for Medical Sciences
16 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 16 shared publications
Maria Almeida
University of Arkansas for Medical Sciences
15 shared publications
In database
- 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 15 shared publications
Jeff D. Thostenson
University of Arkansas for Medical Sciences
12 shared publications
In database
- 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
- Cortical bone loss caused by glucocorticoid excess requires RANKL production by osteocytes and is associated with reduced OPG expression in mice
Showing 5 of 12 shared publications
Intawat Nookaew
University of Arkansas for Medical Sciences
10 shared publications
In database
- Stimulation of Piezo1 by mechanical signals promotes bone anabolism
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Piezo1 stimulates mitochondrial function via cAMP signaling
- 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
Showing 5 of 10 shared publications
M. Piemontese
University of Arkansas for Medical Sciences (US)
9 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
- Old age causes de novo intracortical bone remodeling and porosity in mice
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Osteocyte-derived RANKL is a critical mediator of the increased bone resorption caused by dietary calcium deficiency
Showing 5 of 9 shared publications
Robert S. Weinstein
Central Arkansas Veterans Healthcare System (US)
7 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
- 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
Showing 5 of 7 shared publications
Stavros C. Manolagas
Central Arkansas Veterans Healthcare System
7 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
- 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
Showing 5 of 7 shared publications
Ha‐Neui Kim
University of Arkansas for Medical Sciences
6 shared publications
In database
- Old age causes de novo intracortical bone remodeling and porosity in mice
- Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence
- Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone
- Piezo1 stimulates mitochondrial function via cAMP signaling
- The Aging Landscape by scRNAseq of Mesenchymal Lineage Cells in Mouse Bone
Showing 5 of 6 shared publications
Robert L. Jilka
5 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
- Old age causes de novo intracortical bone remodeling and porosity in mice
- Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence
Joseph J. Goellner
University of Arkansas for Medical Sciences
5 shared publications
In database
- Osteocytes, not Osteoblasts or Lining Cells, are the Main Source of the RANKL Required for Osteoclast Formation in Remodeling Bone
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- A DNA Segment Spanning the Mouse Tnfsf11 Transcription Unit and Its Upstream Regulatory Domain Rescues the Pleiotropic Biologic Phenotype of the RANKL Null Mouse
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Keisha M. Cawley
University of Arkansas for Medical Sciences (US)
5 shared publications
- Soluble RANKL contributes to osteoclast formation in adult mice but not ovariectomy-induced bone loss
- Osteocyte RANKL is required for cortical bone loss with age and is induced by senescence
- Local Production of Osteoprotegerin by Osteoblasts Suppresses Bone Resorption
- Deletion of a putative promoter-proximal Tnfsf11 regulatory region in mice does not alter bone mass or Tnfsf11 expression in vivo
- Osteoblasts Suppress Bone Resorption Via Production of Osteoprotegerin
Visanu Wanchai
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
- Elevation of master autophagy regulator Tfeb in osteoblast lineage cells increases bone mass and strength
- A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone
- A transcriptomic-driven segmentation and cell simulation framework for high-resolution spatial transcriptomics and cell-cell communication
- Protocol for the enrichment of endosteal and periosteal mesenchymal cells from murine bone for single-cell transcriptome analysis
Qiang Fu
University of Arkansas for Medical Sciences
4 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
- 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
Li Han
University of Arkansas for Medical Sciences (US)
4 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
- Author response: Stimulation of Piezo1 by mechanical signals promotes bone anabolism
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