Rdh11, a retinol dehydrogenase, is an NADPH-dependent retinaldehyde reductase. It functions in the visual cycle, particularly in the oxidation of 11-cis-retinol to 11-cis-retinal in the retinal pigment epithelium (RPE), and also contributes to retinol homeostasis in extraocular tissues like the liver and testis [1,2,3]. It has dual specificity for both cis-and trans-retinoid substrates and may be involved in all-trans-and 9-cis-retinoic acid production [4].

In Rdh11 knockout mice, several phenotypes were observed. Rdh11 -/- embryos from Rdh11 -/- dams had elevated levels of embryonic retinyl esters [1]. Rdh11 -/- mice showed delayed dark adaptation, indicating its role in regenerating visual pigment by complementing RDH5 as an 11-cis-RDH in RPE cells [2]. In addition, microsomes from the testes and livers of Rdh11 -/- mice had lower rates of all-trans-retinaldehyde conversion to all-trans-retinol, and these tissues had lower levels of all-trans-retinol under a vitamin A-deficient diet, suggesting its essential role in maintaining retinol homeostasis in these tissues [3].

In conclusion, Rdh11 is crucial for visual processes, especially dark adaptation, and for maintaining retinol homeostasis in both ocular and extraocular tissues. The study of Rdh11 knockout mouse models has provided valuable insights into its functions, which may be relevant to understanding certain retinopathies and metabolic disorders related to vitamin A metabolism [1,2,3].