The DOI matches its Crossref record; 22 of the 22 references it cites were found in a registry or an index.
Smoking and impaired bone healing: will activation of cholinergic anti-inflammatory pathway be the bridge?
Open accessAbstract
Purpose This review was written to analyse the potential role of the cholinergic anti-inflammatory pathway in smoking-induced impairment of the bone healing process.Methods Literature in PubMed was reviewed by entering the following keywords "smoking AND bone healing", "cholinergic anti-inflammatory pathway AND tumour necrosis factor", "tumour necrosis factor AND bone healing". All the related papers were recruited and carefully selected according to the content of this paper.Results Literature review indicated that tumour necrosis factor alpha (TNF-α) plays a pivotal role in the fracture healing process. In brief, TNF-α may accelerate the endochondral ossification process by increasing matrix metalloproteinases (MMPs) level, chondrocyte apoptosis, as well as osteoclast formation, therefore reducing the cartilaginous stage leading to the acceleration of fracture healing. Nicotine is the main effective ingredient of tobacco, which has been found to inhibit the secretion of TNF-α through activation of the cholinergic anti-inflammatory pathway.Conclusions It is reasonable to believe that the nicotine in tobacco at least partly contributes to the delayed fracture healing by inhibiting TNF-α secretion through the activation of the cholinergic anti-inflammatory pathway. An in-depth study of this issue will contribute to the clinical treatment of nonunion, as well as the development of new therapies to accelerate bone healing.
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Nicotine can at least partially contribute to delayed fracture healing by inhibiting TNF-α secretion through activation of the cholinergic anti-inflammatory pathway, via the α7 nicotinic acetylcholine receptor, activation of JaK2-STAT3, inhibition of NF-κB, and reduced TNF-α production, leading to a prolonged soft callus stage and decreased migration of mesenchymal stem cells.
“In particular, the nicotine released from smoking may act through the α7 nicotinic acetylcholine receptor (α7 nAChR) and activate the anti-inflammatory pathways, thus causing activation of the JaK2-STAT3 signaling pathway and inhibition of the NF-κB signaling pathway. As a result, the production of TNF-α is significantly reduced, which can lead to a prolonged soft callus stage and a decrease in”
From Skeletal System Biology and Smoke Damage: From Basic Science to Medical Clinic (2021) · cites this paper as [65]
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Skeletal System Biology and Smoke Damage: From Basic Science to Medical Clinic
Tarantino, U., Cariati, I., Greggi, C., Gasbarra, E., Belluati, A., Ciolli, L., Maccauro, G., Momoli, A., Ripanti, S., Falez, F., et al. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22126629 · Cited by 52
Metadata
- Authors
- Chen, Y., Guo, Q., Pan, X., Qin, L., & Zhang, P.
- Affiliations
- Army Medical University (CN)
- Chinese University of Hong Kong (HK)
- Chinese Academy of Sciences (CN)
- Corresponding author
- Zhang, Peng
- Venue
- International Orthopaedics
- Published
- 2011-03-16
- Volume
- 35
- Issue
- 9
- Pages
- 1267-1270
- ISSN
- 0341-2695 (ISSN-L)
- 1432-5195
- PMC
- PMC3167453
- OpenAlex
- W2047339318
- Cited by
- 52
- References
- 22
- Citations by year
- 2026: 4 · 2025: 1 · 2024: 2 · 2023: 2 · 2022: 3 · 2021: 5 · 2020: 8 · 2019: 1 · 2018: 4 · 2016: 5 · 2015: 7 · 2014: 2 · 2013: 6 · 2012: 2
- FWCI
- 2.40
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- International Orthopaedics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81000786)
- Topics
- Health Sciences › Medicine › Orthopedics and Sports Medicine › Bone fractures and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
- Health Sciences › Medicine › Surgery › Wound Healing and Treatments
- Keywords
- smoking, bone regeneration, fracture healing, cholinergic anti-inflammatory pathway, TNF-α, nicotine, endochondral ossification, matrix metalloproteinases, chondrocyte apoptosis, osteoclastogenesis, nonunion, delayed fracture healing
- MeSH terms
- Bone Regeneration, Humans, Inflammation, Nicotine, Osteoblasts, Osteogenesis, Smoking, Tumor Necrosis Factor-alpha, Fracture Healing, Cholinergic Agonists, PubMed
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