Sepsis triggered oxidative stress-inflammatory axis: the pathobiology of reprogramming in the normal sleep-wake cycle.
Waleed Hassan Al-MalkiMohammed M GhoneimSultan AlshehriSyed Sarim ImamImran KazmiGaurav GuptaPublished in: Molecular and cellular biochemistry (2022)
In individuals with sepsis-related neurodegenerative illness, sleep and circadian rhythm disturbance are common. The alteration in genomic expression linked with the immune-directed oxidative stress-inflammatory axis is thought to cause these individuals' abnormal sleep. On the other hand, sleep is linked to normal brain activity through common neurotransmitter systems and regulatory mechanisms. Ailments (ranging from cognitive to metabolic abnormalities) are seldom related to aberrant sleep that is made worse by sleep disturbance, which throws off the body's sleep-wake cycle. PubMed/Springer link /Public library of science/ScienceDirect/ Mendeley/Medline and Google Scholar were used to find possibly relevant studies. For the literature search, many keywords were considered, both individually and in combination. 'Sepsis,' 'Epidemiology of sepsis,' 'Sepsis-related hyper inflammation,' 'Relationship of sepsis-associated clock gene expression and relationship of inflammation with the reprogramming of genetic alterations' were some of the key terms utilized in the literature search. Our main objective is to understand better how traumatic infections during sepsis affect CNS processes, particularly sleep, by investigating the pathobiology of circadian reprogramming associated with immune-directed oxidative stress-inflammatory pathway responsive gene expression and sleep-wake behaviour in this study.
Keyphrases
- oxidative stress
- sleep quality
- gene expression
- acute kidney injury
- physical activity
- intensive care unit
- septic shock
- systematic review
- dna damage
- healthcare
- spinal cord injury
- public health
- emergency department
- ischemia reperfusion injury
- depressive symptoms
- diabetic rats
- drug delivery
- atrial fibrillation
- risk factors
- blood brain barrier
- copy number
- long non coding rna
- binding protein