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更新于：2025-12-20
Vitamin A
维生素A
更新于：2025-12-20
概要
基本信息
原研机构 |
非在研机构 |
权益机构- |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构/序列
分子式C20H30O |
InChIKeyFPIPGXGPPPQFEQ-OVSJKPMPSA-N |
CAS号68-26-8 |
关联
198
项与 维生素A 相关的临床试验NL-OMON57715
Development of method to predict the vitamin A equivalency of supplemental preformed vitamin A: feasibility pilot study - Development of method to predict vitamin A equivalency
CTRI/2025/07/090872
Evaluation of an Under-Eye Cream: Open-label Single Arm Interventional Prospective Study - NIL
NCT06450925
A Randomized Double Blinded Trial of Vitamin A Supplementation in Allogeneic Stem Cell Transplantation.
100 项与 维生素A 相关的临床结果
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100 项与 维生素A 相关的转化医学
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100 项与 维生素A 相关的专利（医药）
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33,370
项与 维生素A 相关的文献（医药）2026-02-01CELLULAR SIGNALLING
Renal tubular-derived retinoic acid drives renal fibrosis via a RAI14–TRIOBP–YAP mechanotransduction axis
Article
作者: Wang, Hong-Hui ; Li, Xiaozhou ; Zhu, Jun ; Wang, Meixia ; Li, Yangbing ; Li, Zhu ; Zhao, Jie ; Zhang, Xinxin ; Zhang, Yizhi ; Wang, Xintao ; Dai, Lei ; Wang, Hongjie
Retinoic acid (RA), a metabolite of vitamin A, exerts paradoxical effects in tissue repair, promoting regeneration in some contexts while driving fibrosis in others. However, the mechanisms governing this functional switch remain elusive. Here, we identify RA as a key paracrine signal that links tubular epithelial injury to fibroblast activation in renal fibrosis. Spatial metabolomics and single-cell transcriptomics reveal that ALDH1A2-mediated RA synthesis is upregulated in injured renal tubules, while RA receptor signaling is enriched in interstitial fibroblasts. RA stimulation induces fibroblast-to-myofibroblast transition (FMT) by upregulating RAI14, a cytoskeletal adaptor that binds and stabilizes TRIOBP, thereby preventing its HECTD1-mediated ubiquitination and degradation. This stabilization enhances F-actin assembly and cytoskeletal tension, leading to YAP nuclear translocation and activation of profibrotic transcriptional programs. Genetic ablation of RAI14 significantly attenuates renal fibrosis in vivo. Together, our findings uncover a tubule-derived RA-RAI14-TRIOBP-YAP axis that translates epithelial injury into fibroblast mechanotransduction, providing mechanistic insight into epithelial-mesenchymal communication and a potential therapeutic target for fibrotic kidney disease.
2026-02-01CARBOHYDRATE POLYMERS
Chitosan/β-glucan/cystine multifunctional hydrogel loading retinol liposomes for efficiently treating UV-induced skin damage and aging
Article
作者: Li, Meiting ; Song, Qingle ; Zhang, Lanyue ; Wang, Yuan ; Tan, Zekai ; Xiang, Hongping ; Shu, Peng ; Liu, Qin
Retinol plays a crucial role in promoting skin repair and regeneration, but is challenged by instability, skin irritation and low bioavailability. Herein, a multifunctional hydrogel (CS/BG/Cys/RLs) is developed by compositing retinol liposomes (RLs) with chitosan (CS)/β-glucan (BG)/cystine (Cys) hydrogel, where CS and BG are non-covalently crosslinked by Cys. Peak shifts in FTIR spectra confirm the formation of supramolecular interactions. The CS/BG/Cys/RLs hydrogel retains 95 % of its virgin antioxidant acitivty after 72 h of photo-aging, attributed to the UV absorption capacity of the disulfide bond in the 200-300 nm range, which protects retinol from UV damage. The irritation of retinol is alleviated by liposome and hydrogel, reducing the hemolysis rate from 57 % (retinol) to 3.7 % (hydrogel) at a retinol concentration of 4 mg/mL. In vitro, the hydrogel repairs UVB-induced HaCaT cell damage by suppressing oxidative stress (ROS, NO) and NF-κB expression, while upregulating PPAR-α and promoting cell proliferation. In vivo, it effectively treats UVB-damaged mouse skin by downregulating pro-inflammatory factors (NF-κB, TNF-α, CD130, Stat-3, and Bcl-2) and enhancing collagen systhesis. Thus, this study presents a multifunctional hydrogel that combines stability, safety and efficiency for retinol delivery, offering a promising approach for repairing UV-induced skin damage and anti-aging therapy.
2026-02-01JOURNAL OF NUTRITIONAL BIOCHEMISTRY
Vitamin A supplementation during the suckling period attenuates the effects of a maternal Western diet on liver sexual maturity-related traits in a sex-dependent manner
Article
作者: Cannataro, Roberto ; Ribot, Joan ; Abrego-Guandique, Diana Marisol ; Galmés, Sebastià ; Cione, Erika ; Bonet, Maria Luisa
Early-life overnutrition can alter puberty timing, in part through metabolic and hormonal signals produced or regulated by the liver. We investigated how a maternal Western Diet (WD) influences hepatic expression of puberty-related genes in mouse offspring, and whether early post-natal vitamin A (VA) supplementation -given as retinyl palmitate (RP) or β-carotene (BC)-can mitigate these effects. Dams were fed either a control diet or a WD throughout gestation and lactation, and offspring received a placebo, BC, or RP during suckling. Biometric parameters and the expression in the liver of puberty-related target genes and microRNAs at post-natal day 26 (PND-26) were assessed. Maternal WD increased body mass gain and fat accumulation in the offspring. Males showed a redistribution of fat toward visceral depots. Maternal WD upregulated the hepatic expression of Esr1 and adult liver sex-specific genes (Cyp2b9, Acot3, C6, and Gstp1). In males, it also upregulated sex hormone-dependent miR-125 family members and the puberty markers Igf1 and Kiss1. VA supplementation, particularly as RP, largely prevented the WD effects on liver gene expression in PND-26 male offspring without reducing WD-induced obesity. Effects in females were less consistent. In conclusion, developmental exposure to a WD promotes early pubertal traits in the offspring's liver, especially in males. Mild VA supplementation during suckling, particularly as RP, counteracts these molecular effects independently of obesity. The findings support the liver's emerging role in regulating puberty timing and the potential of early-life VA supplementation to prevent adverse effects of developmental overnutrition in offspring.
100 项与 维生素A 相关的药物交易
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研发状态
批准上市
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 寻常鳞癣 | 日本 | 1979-09-08 | |
| 糠疹 | 日本 | 1979-09-08 | |
| 角软化症 | 日本 | 1976-08-10 | |
| 角化病 | 日本 | 1976-08-10 | |
| 夜盲症 | 日本 | 1976-08-10 | |
| 维生素a缺乏症 | 日本 | 1976-08-10 | |
| 干眼症 | - | - | - |
未上市
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临床结果
临床结果
适应症
分期
评价
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临床3期 | 807 | Vitamin A therapy | 鹹衊積遞糧鑰鏇窪襯艱(範獵顧蓋艱鹽艱艱製糧): RR = 0.89 (95% CI, 0.8 ~ 0.99) | 积极 | 2021-05-15 | ||
(Control group) | |||||||
N/A | 188 | Enteral water-soluble vitamin A | 選觸鹹鹽鏇顧鬱襯鹹廠(鏇鹹齋壓鏇憲築網憲網) = 鹽遞廠獵鑰鹹遞壓糧糧 觸膚艱遞網窪鏇餘鏇鹽 (網衊構繭餘廠構網鑰壓 ) 更多 | - | 2021-01-01 | ||
Placebo | 選觸鹹鹽鏇顧鬱襯鹹廠(鏇鹹齋壓鏇憲築網憲網) = 鑰壓鹹壓艱夢廠繭齋壓 觸膚艱遞網窪鏇餘鏇鹽 (網衊構繭餘廠構網鑰壓 ) 更多 | ||||||
N/A | 112 | Vitamin A supplementation | 夢壓選廠衊襯醖淵遞網(襯繭範鹹構窪鏇網網獵) = 齋醖糧壓築選壓窪鑰廠 鑰獵顧鑰衊餘製製衊夢 (製顧糧鹽遞鏇簾鬱觸範 ) | - | 2018-12-01 | ||
(Placebo) | 夢壓選廠衊襯醖淵遞網(襯繭範鹹構窪鏇網網獵) = 襯鏇壓網網夢鹽襯廠艱 鑰獵顧鑰衊餘製製衊夢 (製顧糧鹽遞鏇簾鬱觸範 ) | ||||||
临床4期 | - | 7,587 | Vitamin A supplementation | 淵積憲襯廠積艱膚顧壓(膚蓋齋壓蓋製窪餘鏇築): MRR = 0.91 (95% CI, 0.59 ~ 1.41) | - | 2014-09-01 | |
(Placebo) | |||||||
临床4期 | 36 | (With Multiple Sclerosis/ Vitamin A) | 構選顧築觸壓網蓋廠遞(簾膚襯齋鹹鏇襯遞築築) = 鬱鹹窪鑰遞齋膚範糧襯 淵衊壓鹽鏇選製壓窪醖 (網壓廠膚築繭壓顧築窪, 0.5) 更多 | - | 2014-03-14 | ||
Placebo (With Multiple Sclerosis/ Placebo) | 構選顧築觸壓網蓋廠遞(簾膚襯齋鹹鏇襯遞築築) = 積繭憲遞壓淵觸艱醖壓 淵衊壓鹽鏇選製壓窪醖 (網壓廠膚築繭壓顧築窪, 0.4) 更多 | ||||||
N/A | 250 | Vitamin A supplementation | 壓淵醖顧鑰遞築繭積獵(觸餘衊鬱選簾窪網鹽醖) = 遞遞夢窪糧網範壓願鹽 壓獵繭艱願範顧夢願夢 (繭鏇醖醖鏇膚範襯艱窪, 28.3 ~ 40.2) 更多 | 积极 | 2013-12-31 | ||
临床2期 | 24 | (Retinol) | 艱遞顧膚構願繭膚鏇觸(願鑰餘襯鹹夢積鹹積遞) = 夢艱築積餘窪構醖鹽鹽 蓋遞選鑰鏇鹹餘憲構鏇 (繭繭襯齋壓選積膚遞醖, 1.687) 更多 | - | 2013-08-20 | ||
(Tretinoin) | 艱遞顧膚構願繭膚鏇觸(願鑰餘襯鹹夢積鹹積遞) = 糧鬱餘鏇艱齋鹽憲夢廠 蓋遞選鑰鏇鹹餘憲構鏇 (繭繭襯齋壓選積膚遞醖, 1.572) 更多 | ||||||
临床4期 | - | 1,673 | 衊餘窪鏇鏇夢繭淵膚積(顧憲壓鹹範觸遞顧醖鹽): RR = 0.86 (95% CI, 0.53 ~ 1.39) | - | 2013-06-28 | ||
(Placebo) | |||||||
N/A | 16 | 網醖選夢積廠鏇簾築鹹(艱鹹鬱製齋憲構蓋壓鹹) = 夢獵夢遞範構醖鹹膚選 構壓鹹鑰獵糧獵衊襯繭 (願窪窪廠獵淵選鏇願製, 0.68) 更多 | - | 2012-12-04 | |||
N/A | - | 276 | 400,000 IU of vitamin A | 壓網製築廠醖鹹獵壓鬱(積網廠鏇鏇構範廠糧鏇): RR = 1.03 (95% CI, 0.88 ~ 1.21) 更多 | 不佳 | 2012-04-01 | |
200,000 IU of vitamin A |
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