TY - JOUR
T1 - Non-coding RNAs and Exosomal Non-coding RNAs in Traumatic Brain Injury
T2 - the Small Player with Big Actions
AU - Mohamadzadeh, Omid
AU - Hajinouri, Mahsasadat
AU - Moammer, Farzaneh
AU - Tamehri Zadeh, Seyed Saeed
AU - Omid Shafiei, Ghoncheh
AU - Jafari, Ameneh
AU - Ostadian, Amirreza
AU - Talaei Zavareh, Sayyed Alireza
AU - Hamblin, Michael R.
AU - Yazdi, Arezoo Jafarian
AU - Sheida, Amirhossein
AU - Mirzaei, Hamed
N1 - Publisher Copyright:
© 2023, The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.
PY - 2023/7
Y1 - 2023/7
N2 - Nowadays, there is an increasing concern regarding traumatic brain injury (TBI) worldwide since substantial morbidity is observed after it, and the long-term consequences that are not yet fully recognized. A number of cellular pathways related to the secondary injury in brain have been identified, including free radical production (owing to mitochondrial dysfunction), excitotoxicity (regulated by excitatory neurotransmitters), apoptosis, and neuroinflammatory responses (as a result of activation of the immune system and central nervous system). In this context, non-coding RNAs (ncRNAs) maintain a fundamental contribution to post-transcriptional regulation. It has been shown that mammalian brains express high levels of ncRNAs that are involved in several brain physiological processes. Furthermore, altered levels of ncRNA expression have been found in those with traumatic as well non-traumatic brain injuries. The current review highlights the primary molecular mechanisms participated in TBI that describes the latest and novel results about changes and role of ncRNAs in TBI in both clinical and experimental research.
AB - Nowadays, there is an increasing concern regarding traumatic brain injury (TBI) worldwide since substantial morbidity is observed after it, and the long-term consequences that are not yet fully recognized. A number of cellular pathways related to the secondary injury in brain have been identified, including free radical production (owing to mitochondrial dysfunction), excitotoxicity (regulated by excitatory neurotransmitters), apoptosis, and neuroinflammatory responses (as a result of activation of the immune system and central nervous system). In this context, non-coding RNAs (ncRNAs) maintain a fundamental contribution to post-transcriptional regulation. It has been shown that mammalian brains express high levels of ncRNAs that are involved in several brain physiological processes. Furthermore, altered levels of ncRNA expression have been found in those with traumatic as well non-traumatic brain injuries. The current review highlights the primary molecular mechanisms participated in TBI that describes the latest and novel results about changes and role of ncRNAs in TBI in both clinical and experimental research.
KW - Exosome
KW - Long non-coding RNAs
KW - MicroRNAs
KW - Non-coding RNA
KW - Traumatic brain injury
UR - http://www.scopus.com/inward/record.url?scp=85151541890&partnerID=8YFLogxK
U2 - 10.1007/s12035-023-03321-y
DO - 10.1007/s12035-023-03321-y
M3 - Review article
C2 - 37020123
AN - SCOPUS:85151541890
SN - 0893-7648
VL - 60
SP - 4064
EP - 4083
JO - Molecular Neurobiology
JF - Molecular Neurobiology
IS - 7
ER -