AKR1B1/ALR2 Cancer Research Results

AKR1B1/ALR2, Aldo-Keto Reductase Family 1 Member B1 / Aldose Reductase: Click to Expand ⟱
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Type:

AKR1B1 - Aldo-Keto Reductase Family 1 Member B1 / Aldose Reductase

Abbreviation: AKR1B1, AR, ALR2, Aldose Reductase

Type: NADPH-dependent aldo-keto reductase / polyol pathway enzyme

Function: AKR1B1 catalyzes the NADPH-dependent reduction of glucose to sorbitol in the polyol pathway and also reduces reactive aldehydes and other carbonyl compounds. It contributes to redox balance, glucose metabolism, inflammatory signaling, prostaglandin metabolism, and cellular responses to oxidative stress.

Cancer: ↑ Frequently overexpressed or functionally activated in cancer. Increased AKR1B1 can promote inflammatory signaling, proliferation, survival, epithelial-mesenchymal transition, migration, invasion, and treatment resistance through pathways involving NF-κB, AKT/mTOR, ROS-responsive signaling, and prostaglandin metabolism. AKR1B1 inhibition has shown predominantly anticancer effects in preclinical studies.
Scientific Papers found: Click to Expand⟱
8054- KAE,    Kaempferol Improves Alzheimer's Disease by Inhibiting Neuronal Ferroptosis via Activating GPX4/AKR1C3 Signaling Pathway
- vitro+vivo, AD, NA
*AKR1B10↝, Kaempferol treatment facilitated the expression of AKR1B1 in PC12 cells exposed to Aβ1–42
*MDA↓, Kaempferol treatment mitigated the Aβ1–42‐induced increases in Fe2+, MDA, and lipid ROS and Aβ1–42‐induced decreases in GSH synthesis and SOD activity.
*ROS↓,
*GSH↑,
*SOD↑,
*GPx4↑, The reduction in ferroptosis‐related proteins (GPX4, NQO1, SLC7A11, AKR1C1, and AKR1C3) and the inhibition of Nrf2 nuclear translocation and Nrf2/HO‐1 signaling caused by Aβ1–42 were also reversed by kaempferol.
*NQO1↑,
*xCT/SLC7A11↑,
*NRF2↑,
*HO-1↑,
*cognitive↑, In vivo studies revealed that kaempferol improved cognitive impairments, reduced deposition of Aβ and p‐Tau, and alleviated neuronal ferroptosis in the hippocampal tissues of an AD mouse model
*Aβ↓,
*p‑tau↓,
*Ferroptosis↓,
*AKR1C3/17β-HSD5/PGF Synthase↑, inhibiting neuronal ferroptosis through the activation of the Nrf2/HO‐1/GPX4/AKR1C3 signaling via upregulation of AKR1B1
*AKR1B1/ALR2↑,


Showing Research Papers: 1 to 1 of 1

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 1

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned(tgid=0) ⓘ

AKR1B1/ALR2↑, 1,   AKR1B10↝, 1,   AKR1C3/17β-HSD5/PGF Synthase↑, 1,  

Redox & Oxidative Stress(tgid=1) ⓘ

Ferroptosis↓, 1,   GPx4↑, 1,   GSH↑, 1,   HO-1↑, 1,   MDA↓, 1,   NQO1↑, 1,   NRF2↑, 1,   ROS↓, 1,   SOD↑, 1,   xCT/SLC7A11↑, 1,  

Cell Death(tgid=5) ⓘ

Ferroptosis↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,  
Total Targets: 17

Scientific Paper Hit Count for: AKR1B1/ALR2, Aldo-Keto Reductase Family 1 Member B1 / Aldose Reductase
Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:1752  State#:%  Dir#:2
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