Parisa Varshosaz
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Parisa Varshosaz has a total of 2 co-authors. Here are the top co-authors by number of shared publications:
- Alexander Radu Moise
Medical Sciences Division, Northern Ontario School of Medicine, Sudbury, ON P3E 2C6, Canada
1 shared publication - Catherine O’connor
MD Program, Northern Ontario School of Medicine University, 935 Ramsey Lake Rd., Sudbury, ON P3E 2C6, Canada
1 shared publication
Latest Publications
- Open Access
Mechanisms of Feedback Regulation of Vitamin A Metabolism
Vitamin A is an essential nutrient required throughout life. Through its various metabolites, vitamin A sustains fetal development, immunity, vision, and the maintenance, regulation, and repair of adult tissues. Abnormal tissue levels of the vitamin A metabolite, retinoic acid, can result in detrimental effects which can include congenital defects, immune deficiencies, proliferative defects, and toxicity. For this reason, intricate feedback mechanisms have evolved to allow tissues to generate appropriate levels of active retinoid metabolites despite variations in the level and format, or in the absorption and conversion efficiency of dietary vitamin A precursors. Here, we review basic mechanisms that govern vitamin A signaling and metabolism, and we focus on retinoic acid-controlled feedback mechanisms that contribute to vitamin A homeostasis. Several approaches to investigate mechanistic details of the vitamin A homeostatic regulation using genomic, gene editing, and chromatin capture technologies are also discussed.
Open AccessMechanisms of Feedback Regulation of Vitamin A Metabolism
Vitamin A is an essential nutrient required throughout life. Through its various metabolites, vitamin A sustains fetal development, immunity, vision, and the maintenance, regulation, and repair of adult tissues. Abnormal tissue levels of the vitamin A metabolite, retinoic acid, can result in detrimental effects which can include congenital defects, immune deficiencies, proliferative defects, and toxicity. For this reason, intricate feedback mechanisms have evolved to allow tissues to generate appropriate levels of active retinoid metabolites despite variations in the level and format, or in the absorption and conversion efficiency of dietary vitamin A precursors. Here, we review basic mechanisms that govern vitamin A signaling and metabolism, and we focus on retinoic acid-controlled feedback mechanisms that contribute to vitamin A homeostasis. Several approaches to investigate mechanistic details of the vitamin A homeostatic regulation using genomic, gene editing, and chromatin capture technologies are also discussed.