Ha‐Neui Kim profile photo

Ha‐Neui Kim

Federal Grant PI High Impact

Associate Professor

University of Arkansas for Medical Sciences

faculty

Internal Med, College of Medicine

hkim@uams.edu

29 h-index 82 pubs 3,124 cited

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Biography and Research Information

OverviewAI-generated summary

Ha-Neui Kim's research focuses on the molecular mechanisms underlying bone aging and the bone loss associated with estrogen deficiency. Her work investigates the role of mitochondrial function, specifically the Sirt3 protein and NAD+ levels, in age-related bone deterioration. Kim also studies the impact of reactive oxygen species on bone cell physiology and pathophysiology. Her federally funded research includes an NIH grant where she is the PI, investigating the role of mitochondrial quality control in bone homeostasis and disease. She also co-PIs an NIH grant focused on the antagonism of RANKL signaling by estrogen in osteoclasts.

Kim's laboratory has published on the cellular identity of mesenchymal cells involved in bone remodeling and the effects of specific genes, such as Mmp13, in mesenchymal cells on bone mass and cortical bone loss. Her research also extends to the influence of ionizing radiation on osteoclast function and subsequent bone loss in male mice. She is recognized as a high-impact researcher, with 82 publications and over 3,124 citations, and an h-index of 29. Her work is supported by two federal grants totaling $712,654.

Kim actively collaborates with researchers at the University of Arkansas for Medical Sciences, including Maria Almeida, Aaron Warren, Charles A. O’Brien, and Stavros C. Manolagas, with whom she has co-authored numerous publications. She maintains an active laboratory website to share her research findings.

Metrics

  • h-index: 29
  • Publications: 82
  • Citations: 3,124

Selected Publications

  • Deletion of the scavenger receptor Scarb1 in osteoblast progenitors and myeloid cells does not affect bone mass (2025) DOI
  • The Aging Landscape by <scp>scRNAseq</scp> of Mesenchymal Lineage Cells in Mouse Bone (2025) DOI
  • Estrogens protect bone mass by inhibiting NAD <sup>+</sup> metabolism in osteoclasts (2025) DOI
  • Deletion of the scavenger receptor <i>Scarb1</i> in osteoblast progenitors and myeloid cells does not affect bone mass (2025) DOI
  • Sirtuin-3 promotes osteoclast maturation and bone loss by regulating mitochondrial ROS production during ionizing radiation exposure (2025) DOI
  • Mechanisms of mitochondrial reactive oxygen species action in bone mesenchymal cells (2025) DOI
  • Oestradiol and osteoclast differentiation: Effects on p53 and mitochondrial metabolism (2024) DOI
  • Refining the identity of mesenchymal cell types associated with murine periosteal and endosteal bone (2024) DOI
  • TMI-Based Dose-Escalated Bone Marrow Transplantation Can Help Preserve the Bone Marrow Microenvironment and Reduce Cellular Senescence in Old Mice (2023) DOI
  • A framework for defining mesenchymal cell types associated with murine periosteal and endosteal bone (2023) DOI
  • OR27-02 The Bone Anabolic Effect Of An Antibody Blocking Oxidized Phospholipids Is Associated With An Increase In Wnt10b In Osteoblasts. (2023) DOI
  • Peptidylarginine deiminase 2 plays a key role in osteogenesis by enhancing RUNX2 stability through citrullination (2023) DOI
  • Retraction notice to “Deletion of the scavenger receptor Scarb1 in myeloid cells does not affect bone mass” [Bone 170(2023) 116702] (2023) DOI
  • The NAD salvage pathway in mesenchymal cells is indispensable for skeletal development in mice (2023) DOI
  • ECSIT is essential for RANKL-induced stimulation of mitochondria in osteoclasts and a target for the anti-osteoclastogenic effects of estrogens (2023) DOI

Federal Grants 2 $712,654 total

NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases Co-PI Mar 2024 - Feb 2029

Antagonism of RANKL signaling by estrogen in osteoclasts

National Institute of Arthritis and Musculoskeletal and Skin Diseases $409,714 R01
NIH/National Institute of Arthritis and Musculoskeletal and Skin Diseases Contact PI Aug 2022 - Jul 2027

Role of Mitochondrial Quality Control in Bone Homeostasis and Disease

National Institute of Arthritis and Musculoskeletal and Skin Diseases $302,940 R01

Grants & Funding

  • DNA damage in bone cells UAMS Intramural Grant Programs Principal Investigator
  • Antagonism of RANKL signaling by estrogen in osteoclasts NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
  • Role of Mitochondrial Quality Control in Bone Homeostasis and Disease NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
  • Role of FoxOs in Skeletal Homeostasis- Resubmission - Continuation-Continuation - Continuation - Continuation NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Co-Investigator
  • Antagonism of RANKL signaling by estrogen in osteoclasts NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
  • Mechanisms of decreased bone formation with aging NIH/Nat. Inst. of Arthritis & Musculoskeletal & Skin Diseases Principal Investigator
  • Role of Mitochondrial Deacetylase Sirt3 in Skeletal Homeostasis UAMS CMDR Principal Investigator
  • Novel role of immunoproteaseome during renal cold storage and transplantation UAMS College of Medicine Principal Investigator

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