PMID- 38439078
OWN - NLM
STAT- MEDLINE
DCOM- 20240306
LR  - 20240320
IS  - 1478-811X (Electronic)
IS  - 1478-811X (Linking)
VI  - 22
IP  - 1
DP  - 2024 Mar 4
TI  - Role of the NF-kB signalling pathway in heterotopic ossification: biological and 
      therapeutic significance.
PG  - 159
LID - 10.1186/s12964-024-01533-w [doi]
LID - 159
AB  - Heterotopic ossification (HO) is a pathological process in which ectopic bone 
      develops in soft tissues within the skeletal system. Endochondral ossification 
      can be divided into the following types of acquired and inherited ossification: 
      traumatic HO (tHO) and fibrodysplasia ossificans progressiva (FOP). Nuclear 
      transcription factor kappa B (NF-kappaB) signalling is essential during HO. NF-kappaB 
      signalling can drive initial inflammation through interactions with the NOD-like 
      receptor protein 3 (NLRP3) inflammasome, Sirtuin 1 (SIRT1) and AMP-activated 
      protein kinase (AMPK). In the chondrogenesis stage, NF-kappaB signalling can promote 
      chondrogenesis through interactions with mechanistic target of rapamycin (mTOR), 
      phosphatidylinositol-3-kinase (PI3K)/AKT (protein kinase B, PKB) and other 
      molecules, including R-spondin 2 (Rspo2) and SRY-box 9 (Sox9). NF-kappaB expression 
      can modulate osteoblast differentiation by upregulating secreted protein acidic 
      and rich in cysteine (SPARC) and interacting with mTOR signalling, bone 
      morphogenetic protein (BMP) signalling or integrin-mediated signalling under 
      stretch stimulation in the final osteogenic stage. In FOP, mutated ACVR1-induced 
      NF-kappaB signalling exacerbates inflammation in macrophages and can promote 
      chondrogenesis and osteogenesis in mesenchymal stem cells (MSCs) through 
      interactions with smad signalling and mTOR signalling. This review summarizes the 
      molecular mechanism of NF-kappaB signalling during HO and highlights potential 
      therapeutics for treating HO.
CI  - (c) 2024. The Author(s).
FAU - Liu, Fangzhou
AU  - Liu F
AD  - Department of Pathophysiology, School of Basic Medical Sciences, Jiangxi Medical 
      College, Nanchang University, Nanchang, Jiangxi, 330006, China.
AD  - Queen Mary School, Jiangxi Medical College, Nanchang University, Nanchang, 
      Jiangxi Province, 330006, China.
FAU - Zhao, Yike
AU  - Zhao Y
AD  - Department of Pathophysiology, School of Basic Medical Sciences, Jiangxi Medical 
      College, Nanchang University, Nanchang, Jiangxi, 330006, China.
AD  - Queen Mary School, Jiangxi Medical College, Nanchang University, Nanchang, 
      Jiangxi Province, 330006, China.
FAU - Pei, Yiran
AU  - Pei Y
AD  - Department of Pathophysiology, School of Basic Medical Sciences, Jiangxi Medical 
      College, Nanchang University, Nanchang, Jiangxi, 330006, China.
AD  - Queen Mary School, Jiangxi Medical College, Nanchang University, Nanchang, 
      Jiangxi Province, 330006, China.
FAU - Lian, Fengyu
AU  - Lian F
AD  - Department of Pathophysiology, School of Basic Medical Sciences, Jiangxi Medical 
      College, Nanchang University, Nanchang, Jiangxi, 330006, China.
AD  - Queen Mary School, Jiangxi Medical College, Nanchang University, Nanchang, 
      Jiangxi Province, 330006, China.
FAU - Lin, Hui
AU  - Lin H
AD  - Department of Pathophysiology, School of Basic Medical Sciences, Jiangxi Medical 
      College, Nanchang University, Nanchang, Jiangxi, 330006, China. 
      huilin88@ncu.edu.cn.
LA  - eng
GR  - 31900852/National Natural Science Foundation of China/
GR  - 20224ACB206024, 20232BAB206081 and 20232BCJ23008/Natural Science Foundation of 
      Jiangxi Province/
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Review
DEP - 20240304
PL  - England
TA  - Cell Commun Signal
JT  - Cell communication and signaling : CCS
JID - 101170464
RN  - 0 (NF-kappa B)
RN  - 0 (Osteonectin)
RN  - EC 2.7.11.1 (TOR Serine-Threonine Kinases)
SB  - IM
MH  - Humans
MH  - *NF-kappa B
MH  - Osteonectin
MH  - TOR Serine-Threonine Kinases
MH  - Inflammation
MH  - *Ossification, Heterotopic
PMC - PMC10910758
OTO - NOTNLM
OT  - Heterotopic ossification
OT  - Molecular mechanism
OT  - NF-kappab signalling
OT  - Treatment
COIS- The authors have no competing interests.
EDAT- 2024/03/05 00:45
MHDA- 2024/03/06 06:43
PMCR- 2024/03/04
CRDT- 2024/03/04 23:55
PHST- 2023/12/31 00:00 [received]
PHST- 2024/02/13 00:00 [accepted]
PHST- 2024/03/06 06:43 [medline]
PHST- 2024/03/05 00:45 [pubmed]
PHST- 2024/03/04 23:55 [entrez]
PHST- 2024/03/04 00:00 [pmc-release]
AID - 10.1186/s12964-024-01533-w [pii]
AID - 1533 [pii]
AID - 10.1186/s12964-024-01533-w [doi]
PST - epublish
SO  - Cell Commun Signal. 2024 Mar 4;22(1):159. doi: 10.1186/s12964-024-01533-w.