ArticleFrontiers in endocrinology2022
Myeloid cell-derived catecholamines influence bone turnover and regeneration in mice.
Article in Frontiers in endocrinology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Impaired bone healing upon neutrophil-specific adrenoreceptor beta 2 knockout in non-osteoporotic and osteoporotic mice.NPJ Regenerative medicine · 2026Article
- βJBMR plus · 2026Article
- Advances in the regulation of bone metabolism by central nuclei: a new perspective on the brain-bone axis.Frontiers in neuroscience · 2026Review
- Article
- The influence of adrenoceptor blocker treatment on fracture healing in osteoporotic and non-osteoporotic bone.Frontiers in physiology · 2025Article
- Neutrophil-derived catecholamines mediate negative stress effects on bone.Nature communications · 2023Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Catecholamine signaling is known to influence bone tissue as reuptake of norepinephrine released from sympathetic nerves into bone cells declines with age leading to osteoporosis. Further, β-adrenoceptor-blockers like propranolol provoke osteoprotective effects in osteoporotic patients. However, besides systemic adrenal and sympathetic catecholamine production, it is also known that myeloid cells can synthesize catecholamines, especially under inflammatory conditions. To investigate the effects of catecholamines produced by CD11b
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Registered trials
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