Effects of circadian rhythm disruption on retinal physiopathology: Considerations from a consensus of experts.
Mariacristina ParravanoC M EandiMichele FigusMarco LupidiF MenchiniM NicoloV ParisiL TotoFrancesco ViolaStela VujosevicFrancesca AmorosoPublished in: European journal of ophthalmology (2022)
The circadian rhythms originate within the organism and synchronize with cyclic fluctuations in the external environment. It has been demonstrated that part of the human genome is under control of the circadian clock and that a synchronizer that helps to maintain daily rhythms is Melatonin, a neuro-hormone primarily synthesized by the pineal gland during the night. The chronic disruption of circadian rhythm has been linked to many conditions such as obesity, metabolic syndrome, type 2 diabetes, cancer, and neurodegenerative diseases. Studies in the mice showed that the disruption of the retinal circadian rhythm increases the decline during the aging of photoreceptors, accelerating age-related disruption of cone cell structure, function, and viability and that the melatonin receptor deletion seems to influence the health of retinal cells, speeding up their aging. In conclusion, preserving the circadian rhythms could be to add to the prevention and treatment of age-related degenerative retinal diseases, and although additional studies are needed, melatonin could be a valid support to favor this "chronoprotection action".
Keyphrases
- optical coherence tomography
- diabetic retinopathy
- metabolic syndrome
- type diabetes
- atrial fibrillation
- optic nerve
- insulin resistance
- heart rate
- endothelial cells
- high fat diet induced
- healthcare
- public health
- cardiovascular disease
- physical activity
- induced apoptosis
- single cell
- mental health
- weight loss
- gene expression
- stem cells
- papillary thyroid
- case control
- dna methylation
- young adults
- skeletal muscle
- combination therapy
- squamous cell carcinoma
- cardiovascular risk factors
- body mass index
- childhood cancer
- sleep quality
- lymph node metastasis
- endoplasmic reticulum stress
- pi k akt