Melatonin is the main biochronologic molecular mediator of circadian rhythm and sleep. It is also a powerful antioxidant and has roles in other physiologic pathways. Melatonin deficiency is associated with metabolic derangements including glucose and cholesterol dysregulation, hypertension, disordered sleep and even cancer, likely due to altered immunity. Diabetic nephropathy (DN) is a key microvascular complication of both type 1 and 2 diabetes. DN is the end result of a complex combination of metabolic, haemodynamic, oxidative and inflammatory factors. Interestingly, these same factors have been linked to melatonin deficiency. This report will collate in a clinician-oriented fashion the mechanistic link between melatonin deficiency and factors contributing to DN.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7467577 | PMC |
http://dx.doi.org/10.1093/ckj/sfz198 | DOI Listing |
Antioxidants (Basel)
December 2024
Key Laboratory for New Technology Research of Vegetable, Vegetable Research Institute, Guangdong Academy of Agricultural Science, Guangzhou 510640, China.
In plants, calcium (Ca) serves as an essential nutrient and signaling molecule. Melatonin is a biologically active and multi-functional hormone that plays an important role in improving nutrient use efficiency. However, its involvement in plant responses to Ca deficiency remains largely unexplored.
View Article and Find Full Text PDFGenes Dis
March 2025
Pediatric Orthopaedic Hospital, Honghui Hospital, Xi'an Jiaotong University, Xi'an, Shaanxi 710032, China.
Although the pathogenesis and mechanism of congenital skeletal dysplasia are better understood, progress in drug development and intervention research remains limited. Here we report that melatonin treatment elicits a mitigating effect on skeletal abnormalities caused by deficiency. In addition to our previous finding of endoplasmic reticulum stress upon deficiency, we found calcium (Ca) overload jointly contributed to -associated chondrodysplasias.
View Article and Find Full Text PDFJ Pineal Res
November 2024
Faculty of Medicine, Institute for Anatomy II, Goethe University Frankfurt, Frankfurt am Main, Germany.
In mice, variability in adult bone size and density has been observed among common inbred strains. Also, in the group of genes regulating circadian rhythmicity in mice, so called clock genes, changes in body size and skeletal parameters have been noted in knockout mice. Here, we studied the size and density of prominent bones of the axial and appendicular skeleton of clock gene Period-1-deficient (Per1) mice by means of microcomputed tomography.
View Article and Find Full Text PDFPhysiol Plant
December 2024
Jiangsu Key Laboratory of Crop Genomics and Molecular Breeding/Zhongshan Biological Breeding Laboratory/Key Laboratory of Plant Functional Genomics of the Ministry of Education, Agriculture College of Yangzhou University, Yangzhou, China.
The growing utilization of metal oxide nanoparticles (MONPs) presents novel and potential hazards to plants. However, the impacts of MONPs on plants and the mechanisms underlying their tolerance to MONPs remain unclear. In this study, we demonstrated that both CuO and ZnO nanoparticles hindered plant growth and triggered oxidative damage in rice seedlings.
View Article and Find Full Text PDFMetab Brain Dis
December 2024
Research Laboratory, Molecular Bases of Human Pathology, Faculty of Medicine, University of Sfax, Sfax, LR19ES13, Tunisia.
Multiple sclerosis (MS) can induce cardiac autonomic dysfunction identified by a decreased heart rate variability (HRV) which was linked to oxidative stress, vitamin D deficiency and sleep disturbance. Previous MS studies revealed the antioxidant and anti-inflammatory effects of exogenous melatonin, as well as its benefits on sleep and vitamin D. We aimed to investigate the change in HRV, oxidative stress, systemic inflammation and sleep following melatonin supplementation in MS patients.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!