PMID- 34315404
OWN - NLM
STAT- MEDLINE
DCOM- 20220131
LR  - 20220131
IS  - 1689-1392 (Electronic)
IS  - 1425-8153 (Print)
IS  - 1425-8153 (Linking)
VI  - 26
IP  - 1
DP  - 2021 Jul 27
TI  - Burn-induced heterotopic ossification from incidence to therapy: key signaling 
      pathways underlying ectopic bone formation.
PG  - 34
LID - 10.1186/s11658-021-00277-6 [doi]
LID - 34
AB  - Burn injury is one of the potential causes of heterotopic ossification (HO), 
      which is a rare but debilitating condition. The incidence ranges from 3.5 to 5.6 
      depending on body area. Burns that cover a larger percentage of the total body 
      surface area (TBSA), require skin graft surgeries, or necessitate pulmonary 
      intensive care are well-researched risk factors for HO. Since burns initiate such 
      complex pathophysiological processes with a variety of molecular signal changes, 
      it is essential to focus on HO in the specific context of burn injury to define 
      best practices for its treatment. There are numerous key players in the pathways 
      of burn-induced HO, including neutrophils, monocytes, transforming growth 
      factor-beta1-expressing macrophages and the adaptive immune system. The increased 
      inflammation associated with burn injuries is also associated with pathway 
      activation. Neurological and calcium-related contributions are also known. 
      Endothelial-to-mesenchymal transition (EMT) and vascularization are known to play 
      key roles in burn-induced HO, with hypoxia-inducible factor-1 (HIF-1) and 
      vascular endothelial growth factor (VEGF) as potential initiators. Currently, 
      non-steroidal anti-inflammatory drugs (NSAIDs) and radiotherapy are effective 
      prophylaxes for HO. Limited joint motion, ankylosis and intolerable pain caused 
      by burn-induced HO can be effectively tackled via surgery. Effective biomarkers 
      for monitoring burn-induced HO occurrence and bio-prophylactic and 
      bio-therapeutic strategies should be actively developed in the future.
CI  - (c) 2021. The Author(s).
FAU - Hu, Xianglin
AU  - Hu X
AUID- ORCID: 0000-0002-7133-9867
AD  - Department of Musculoskeletal Surgery, Fudan University Shanghai Cancer Center, 
      Shanghai, 200032, China.
AD  - Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 
      200032, China.
FAU - Sun, Zhengwang
AU  - Sun Z
AD  - Department of Musculoskeletal Surgery, Fudan University Shanghai Cancer Center, 
      Shanghai, 200032, China.
AD  - Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 
      200032, China.
FAU - Li, Fengfeng
AU  - Li F
AD  - Department of Orthopedic Surgery, The Second Affiliated Hospital of Guangzhou 
      Medical University, Guangzhou, 510260, China.
FAU - Jiang, Chaoyin
AU  - Jiang C
AD  - Department of Orthopedic Surgery, Shanghai Sixth People's Hospital, Shanghai 
      Jiaotong University , Shanghai, 200233, China. hunball2@163.com.
FAU - Yan, Wangjun
AU  - Yan W
AD  - Department of Musculoskeletal Surgery, Fudan University Shanghai Cancer Center, 
      Shanghai, 200032, China. yanwj@fudan.edu.cn.
AD  - Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 
      200032, China. yanwj@fudan.edu.cn.
FAU - Sun, Yangbai
AU  - Sun Y
AD  - Department of Musculoskeletal Surgery, Fudan University Shanghai Cancer Center, 
      Shanghai, 200032, China. drsunyb@fudan.edu.cn.
AD  - Department of Oncology, Shanghai Medical College, Fudan University, Shanghai, 
      200032, China. drsunyb@fudan.edu.cn.
AD  - Department of Plastic and Reconstructive Surgery, Shanghai Ninth People's 
      Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200011, 
      China. drsunyb@fudan.edu.cn.
LA  - eng
GR  - 81701937, 81672851, and 81872179/national natural science foundation of china/
GR  - (20A200388)/General Scientific Research of Health and Family Planning Commission 
      of Hainan Province (Haikou) in China/
PT  - Letter
PT  - Review
DEP - 20210727
PL  - England
TA  - Cell Mol Biol Lett
JT  - Cellular & molecular biology letters
JID - 9607427
RN  - 0 (Biomarkers)
SB  - IM
MH  - Biomarkers/blood
MH  - Burns/blood/*metabolism/*pathology
MH  - Humans
MH  - Ossification, Heterotopic/blood/metabolism/pathology/*therapy
MH  - Osteogenesis
MH  - Signal Transduction
PMC - PMC8313878
OTO - NOTNLM
OT  - Burn injury
OT  - Heterotopic ossification
OT  - Incidence
OT  - Mechanism
OT  - Risk factor
OT  - Signaling pathway
COIS- The authors declare that they have no conflict of interest.
EDAT- 2021/07/29 06:00
MHDA- 2022/02/01 06:00
PMCR- 2021/07/27
CRDT- 2021/07/28 05:32
PHST- 2021/04/15 00:00 [received]
PHST- 2021/07/20 00:00 [accepted]
PHST- 2021/07/28 05:32 [entrez]
PHST- 2021/07/29 06:00 [pubmed]
PHST- 2022/02/01 06:00 [medline]
PHST- 2021/07/27 00:00 [pmc-release]
AID - 10.1186/s11658-021-00277-6 [pii]
AID - 277 [pii]
AID - 10.1186/s11658-021-00277-6 [doi]
PST - epublish
SO  - Cell Mol Biol Lett. 2021 Jul 27;26(1):34. doi: 10.1186/s11658-021-00277-6.