Target intelligence / Profile preview

Aldo-keto reductase family 7 member A3 (AKR7A3)

Target
AKR7A3
Molecular classification
Enzyme, Aldo-keto reductase, Phase I metabolic enzyme, Oxidoreductase
01

Overview

Aldo-keto reductase family 7 member A3 (AKR7A3) is a cytosolic enzyme and member of the aldo-keto reductase superfamily, which catalyzes the NADPH-dependent reduction of aldehydes and ketones—including toxic products from cellular metabolism and carcinogenic intermediates such as aflatoxin dialdehydes—into less reactive alcohols. This enzymatic activity protects tissues, particularly the liver, from damage and carcinogenic effects. AKR7A3 forms a dimeric quaternary structure and contains a characteristic (\u03b1/\u03b2)8-barrel fold shared by all AKRs, but features unique loop and helix arrangements of the AKR7 subclass. It is encoded on human chromosome 1 and expressed in tissues including stomach, pancreas, and kidney, and is being investigated for its roles in cancer prevention and metabolic disease.

Other names
AKR7A3AFAR2Aflatoxin aldehyde reductaseAflatoxin B1 aldehyde reductase 1aflatoxin aldehyde reductase member 3
02

Mechanism of action

Reduction of toxic aldehydes and ketones to less reactive and non-toxic alcohol forms using NADPH as a cofactor. Metabolic detoxification via enzymatic catalysis, potentially protecting cells (especially liver) from genotoxic damage.

03

Biological functions

Detoxification of aldehydes and ketonesProtection against toxic and carcinogenic effects of aflatoxin B1NADPH-dependent oxidoreductionCellular response to metabolic stress
04

Disease associations

Cancer (especially related to carcinogen metabolism and protection against aflatoxin B1, a liver carcinogen)Developmental Dysplasia of the Hip 1 (gene association)Cytochrome P450 Oxidoreductase Deficiency (gene association)May play indirect roles in liver diseases and other conditions involving carbonyl stress
05

Safety considerations

Therapeutic modulation of AKR7A3 may risk alteration in essential detoxification mechanisms, possibly leading to accumulation of toxic aldehydesInhibition or knockout could increase susceptibility to hepatotoxicity and carcinogenesis from substances such as aflatoxin B1No drug-related toxicities are directly linked, but therapeutic manipulation must consider the enzyme's homeostatic role
06

Interacting drugs

No major clinical drugs directly listed as binding or inhibiting AKR7A3, but compounds interacting with aflatoxin metabolism or aldehyde detoxification could be relevant

1 more in the full profile.

07

Biomarkers

Expression levels of AKR7A3 may serve as indicators of metabolic capacity for aldehyde detoxification or susceptibility to aflatoxin-induced toxicityNo established routine clinical biomarkers, but expression in tumors or liver tissue may have prognostic value

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