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Role of RNA polymerase III transcription and regulation in ischaemic stroke. | LitMetric

AI Article Synopsis

  • Ischaemic stroke leads to significant neuronal damage due to a lack of glucose and oxygen, causing serious disabilities and even death.
  • RNA polymerase III (Pol III) is crucial for protein synthesis in neurons, but its activity is highly affected during ischaemic stress, which impairs brain function.
  • Research indicates that Pol III plays different roles in the brain, such as protecting neurons in the acute phase of a stroke and aiding recovery later on, with the mTOR-MAF1 signaling pathway showing promise for enhancing both neuroprotection and repair.

Article Abstract

Ischaemic stroke is a leading cause of death and life-long disability due to neuronal cell death resulting from interruption of glucose and oxygen supplies. RNA polymerase III (Pol III)-dependent transcription plays a central role in protein synthesis that is necessary for normal cerebral neuronal functions, and the survival and recovery under pathological conditions. Notably, Pol III transcription is highly sensitive to ischaemic stress that is known to rapidly shut down Pol III transcriptional activity. However, its precise role in ischaemic stroke, especially during the acute and recovery phases, remains poorly understood. The microenvironment within the ischaemic brain undergoes dynamic changes in different phases after stroke. Emerging evidence highlights the distinct roles of Pol III transcription in neuroprotection during the acute phase and repair during the recovery phase of stroke. Additionally, investigations into the mTOR-MAF1 signalling pathway, a conserved regulator of Pol-III transcription, reveal its therapeutic potential in enhancing acute phase neuroprotection and recovery phase repair.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11457610PMC
http://dx.doi.org/10.1080/15476286.2024.2409554DOI Listing

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