PMID- 35806192
OWN - NLM
STAT- MEDLINE
DCOM- 20220712
LR  - 20220716
IS  - 1422-0067 (Electronic)
IS  - 1422-0067 (Linking)
VI  - 23
IP  - 13
DP  - 2022 Jun 28
TI  - Neuroimmune Mechanisms Underlying Neuropathic Pain: The Potential Role of 
      TNF-alpha-Necroptosis Pathway.
LID - 10.3390/ijms23137191 [doi]
LID - 7191
AB  - The neuroimmune mechanism underlying neuropathic pain has been extensively 
      studied. Tumor necrosis factor-alpha (TNF-alpha), a key pro-inflammatory cytokine 
      that drives cytokine storm and stimulates a cascade of other cytokines in 
      pain-related pathways, induces and modulates neuropathic pain by facilitating 
      peripheral (primary afferents) and central (spinal cord) sensitization. 
      Functionally, TNF-alpha controls the balance between cell survival and death by 
      inducing an inflammatory response and two programmed cell death mechanisms 
      (apoptosis and necroptosis). Necroptosis, a novel form of programmed cell death, 
      is receiving increasing attraction and may trigger neuroinflammation to promote 
      neuropathic pain. Chronic pain is often accompanied by adverse pain-associated 
      emotional reactions and cognitive disorders. Overproduction of TNF-alpha in 
      supraspinal structures such as the anterior cingulate cortex (ACC) and 
      hippocampus plays an important role in pain-associated emotional disorders and 
      memory deficits and also participates in the modulation of pain transduction. At 
      present, studies reporting on the role of the TNF-alpha-necroptosis pathway in 
      pain-related disorders are lacking. This review indicates the important research 
      prospects of this pathway in pain modulation based on its role in anxiety, 
      depression and memory deficits associated with other neurodegenerative diseases. 
      In addition, we have summarized studies related to the underlying mechanisms of 
      neuropathic pain mediated by TNF-alpha and discussed the role of the 
      TNF-alpha-necroptosis pathway in detail, which may represent an avenue for future 
      therapeutic intervention.
FAU - Duan, Yi-Wen
AU  - Duan YW
AD  - Pain Research Center and Department of Physiology, Zhongshan Medical School, Sun 
      Yat-sen University, 74 Zhongshan Road. 2, Guangzhou 510080, China.
FAU - Chen, Shao-Xia
AU  - Chen SX
AD  - Department of Anesthesiology, Sun Yat-sen University Cancer Center, State Key 
      Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer 
      Medicine, Guangzhou 510060, China.
FAU - Li, Qiao-Yun
AU  - Li QY
AD  - Pain Research Center and Department of Physiology, Zhongshan Medical School, Sun 
      Yat-sen University, 74 Zhongshan Road. 2, Guangzhou 510080, China.
FAU - Zang, Ying
AU  - Zang Y
AD  - Pain Research Center and Department of Physiology, Zhongshan Medical School, Sun 
      Yat-sen University, 74 Zhongshan Road. 2, Guangzhou 510080, China.
LA  - eng
GR  - 81870873/National Natural Science Foundation of China/
GR  - 81801111/National Natural Science Foundation of China/
GR  - 2022A1515012198/the Natural Science Foundation of Guangdong Province of China/
PT  - Journal Article
PT  - Review
DEP - 20220628
PL  - Switzerland
TA  - Int J Mol Sci
JT  - International journal of molecular sciences
JID - 101092791
RN  - 0 (Cytokines)
RN  - 0 (Tumor Necrosis Factor-alpha)
SB  - IM
MH  - Cytokines
MH  - Humans
MH  - Memory Disorders
MH  - Necroptosis
MH  - *Neuralgia/metabolism
MH  - Neuroimmunomodulation
MH  - *Tumor Necrosis Factor-alpha/metabolism
PMC - PMC9266916
OTO - NOTNLM
OT  - necroptosis
OT  - neuroinflammation
OT  - neuropathic pain
OT  - tumor necrosis factor-alpha (TNF-alpha)
COIS- The authors declare no conflict of interest.
EDAT- 2022/07/10 06:00
MHDA- 2022/07/14 06:00
PMCR- 2022/06/28
CRDT- 2022/07/09 01:11
PHST- 2022/05/09 00:00 [received]
PHST- 2022/06/24 00:00 [revised]
PHST- 2022/06/27 00:00 [accepted]
PHST- 2022/07/09 01:11 [entrez]
PHST- 2022/07/10 06:00 [pubmed]
PHST- 2022/07/14 06:00 [medline]
PHST- 2022/06/28 00:00 [pmc-release]
AID - ijms23137191 [pii]
AID - ijms-23-07191 [pii]
AID - 10.3390/ijms23137191 [doi]
PST - epublish
SO  - Int J Mol Sci. 2022 Jun 28;23(13):7191. doi: 10.3390/ijms23137191.