ArticleBlood advances2022
Sickle cell disease promotes sex-dependent pathological bone loss through enhanced cathepsin proteolytic activity in mice.
Article in Blood advances, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Selective AMPKβ1 activation induces fetal hemoglobin in human erythroid cells and sickle cell mice via the noncanonical NRF2 pathway.Science advances · 2025Article
- Hydroxyurea blunts mitochondrial energy metabolism and osteoblast and osteoclast differentiation exacerbating trabecular bone loss in sickle cell mice.Cell death & disease · 2024Article
- Bone Disease among Children with Sickle Cell Disease: A Scoping Review of Incidence and Interventions.Journal of multidisciplinary healthcare · 2024Article
- Proteomic analyses of urinary exosomes identify novel potential biomarkers for early diagnosis of sickle cell nephropathy, a sex-based study.Frontiers in physiology · 2024Article
- Mouse models of sickle cell disease: Imperfect and yet very informative.Blood cells, molecules & diseases · 2024Review
- A study of the influence of genetic variance and sex on the density and thickness of the calvarial bone in collaborative cross mice.Animal models and experimental medicine · 2023Article
- A bone to pick-cellular and molecular mechanisms of bone pain in sickle cell disease.Frontiers in pain research (Lausanne, Switzerland) · 2023Review
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Sickle cell disease (SCD) is the most common hereditary blood disorder in the United States. SCD is frequently associated with osteonecrosis, osteoporosis, osteopenia, and other bone-related complications such as vaso-occlusive pain, ischemic damage, osteomyelitis, and bone marrow hyperplasia known as sickle bone disease (SBD). Previous SBD models have failed to distinguish the age- and sex-specific characteristics of bone morphometry. In this study, we use the Townes mouse model of SCD to assess the pathophysiological complications of SBD in both SCD and sickle cell trait. Changes in bone microarchitecture and bone development were assessed by using high-resolution quantitative micro-computed tomography and the three-dimensional reconstruction of femurs from male and female mice. Our results indicate that SCD causes bone loss and sex-dependent anatomical changes in bone. SCD female mice in particular are prone to trabecular bone loss, whereas cortical bone degradation occurs in both sexes. We also describe the impact of genetic knockdown of cathepsin K- and E-64-mediated cathepsin inhibition on SBD.
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