Alpha-Lipoic-Acid / Hif1a Cancer Research Results

ALA, Alpha-Lipoic-Acid: Click to Expand ⟱
Features: antioxidant, energy production in cell mitochondria
Alpha-Lipoic-Acid: also known as lipoic acid or thioctic acid (reduced form is dihydrolipoic acid).
"Universal antioxidant" because it is both water- and fat-soluble and can neutralize free radicals.
-Treatment sometimes as ALA/N (alpha-lipoic acid/low-dose naltresone)
-Also done in IV
-Decreases ROS production, but also has pro-oxidant role.
Normal adult can take 300 milligrams twice a day with food, but they should always take a B-complex vitamin with it. Because B complex vitamins, especially thiamine, and biotin, and riboflavin, are depleted during this metabolic process.
α-Lipoic acid acts as a chelating agent for metal ions, a quenching agent for reactive oxygen species, and a reducing agent for the oxidized form of glutathione and vitamins C and E.
-It seems a paradox that LA functions as both antioxidant and prooxidant. LA functions the pro-oxidant only in special cancer cells, such as A549 and PC9 cells which should show high-level NRF2 expression and high glycolytic level. Through inhibiting PDK1 to further prohibit NRF2; LA functions as anticancer prooxidant.

α-lipoic acid possesses excellent silver chelating properties.

ALA → ROS ↑ (cancer cells; high dose / stressed mitochondria)
ALA → ROS ↓ (normal cells; low–moderate dose)
same pattern seen with: Vitamin C, Menadione, Quercetin, EGCG, Resveratrol
- ALA acts as pro-Oxidant only in cancer cells:#278 - Pro-Oxidant Dose margin >100uM:#304

- Bioavailability: 80-90%, but conversion to EPA/DHA is 5-10% (and takes longer time).
- AI (Adequate Intake): 1.1-1.6g/day.
- human studies have shown that ALA levels decline significantly with age
- 1g of ALA might achieve 500uM in the blood.
- ALA is poorly soluble, lecithin has been used as an amphiphilic matrix to enhance its bioavailability.
- Pilot studies or observational interventions have used flaxseed supplementation (rich in ALA) in doses providing roughly 3–4 g of ALA daily.
- Flaxseed oil is even more concentrated in ALA – typical 50–60% ALA by weight.
- single walnut may contain 300mg of ALA
- chia oil contains 55-65% ALA.
- α-LA can also be obtained from the diet through the consumption of dark green leafy vegetables and meats
- ALA is more stable in chia seeds, (2grams of ALA per tablespoon)
- ALA degrades when exposed to heat, light, and air. (prone to oxidation)

-Note half-life 1-2 hrs.
BioAv 30-40% from walnuts, 60-80% from supplements. Co-ingestion with fat improves absorption. Both fat and water soluble
Pathways:
- induce ROS production
- ROS↑ related: MMP↓(ΔΨm), ER Stress↑, UPR↑, GRP78↑, Cyt‑c↑, Caspases↑, DNA damage↑,
- Lowers AntiOxidant defense in Cancer Cells: NRF2↓, SOD↓, GSH↓ Catalase↓ HO1↓ GPx↓
- Raises AntiOxidant defense in Normal Cells: ROS↓, NRF2↑, SOD↑, GSH↑, Catalase↑,
- lowers Inflammation : NF-kB↓, COX2↓, Pro-Inflammatory Cytokines : IL-1β↓, TNF-α↓, IL-6↓, IL-8↓
- inhibit Growth/Metastases : TumMeta↓, TumCG↓, EMT↓, MMPs↓, MMP2↓, MMP9↓, IGF-1↓, VEGF↓, FAK↓, NF-κB↓, TGF-β↓, α-SMA↓, ERK↓
- cause Cell cycle arrest : TumCCA↑, cyclin D1↓,
- inhibits Migration/Invasion : TumCMig↓, TumCI↓, TNF-α↓, FAK↓, ERK↓, EMT↓,
- inhibits glycolysis and ATP depletion : HIF-1α↓, PKM2↓, GLUT1↓, LDHA↓, HK2↓, PFKs↓, PDKs↓, ECAR↓, OXPHOS↓, GRP78↑, Glucose↓, GlucoseCon↓
- inhibits angiogenesis↓ : VEGF↓, HIF-1α↓, EGFR↓, Integrins↓,
- small indication of inhibiting Cancer Stem Cells : CSC↓, CD24↓, β-catenin↓,
- Others: PI3K↓, AKT↓, JAK↓, STAT↓, β-catenin↓, AMPK, ERK↓, JNK,
- Synergies: chemo-sensitization, chemoProtective, RadioSensitizer, RadioProtective, Others(review target notes), Neuroprotective, Cognitive, Renoprotection, Hepatoprotective, CardioProtective,

- Selectivity: Cancer Cells vs Normal Cells

Lipoic Acid Cancer Mechanisms

Rank Pathway / Axis Cancer Cells Normal Cells TSF Primary Effect Notes / Interpretation
1 Mitochondrial redox and ROS ↑ mitochondrial ROS; ↔/↓ total ROS (context-dependent) ↓ ROS P/R Apoptosis and redox disruption Central but bidirectional mechanism. HT-29 and A549 models show pro-oxidant ROS-mediated death, whereas MCF-7 and some prostate models show ROS lowering with growth inhibition.
2 PI3K Akt survival signaling ↓ Akt; ↑ p27; ↓ proliferation ↔/↑ Akt (context-dependent) R/G Cell-cycle arrest and apoptosis Breast cancer studies demonstrate suppression of Akt with G1 arrest, Bax/Bcl-2 shift and apoptotic signaling.
3 Mitochondria and MPTP ↑ permeability transition; ↓ membrane potential; ↑ cytochrome c Generally protected from oxidative mitochondrial injury R Intrinsic apoptosis Provides a mechanistic bridge between altered mitochondrial metabolism, ROS production and caspase activation.
4 ER stress CHOP XBP1 ↑ GRP78; ↑ CHOP; ↑ XBP1; ↑ caspases Not established as a therapeutic effect R/G ER-stress-mediated apoptosis Demonstrated prominently in A549 lung cancer cells and substantially dependent on ROS.
5 Ca²⁺ and TRPV1 signaling ↑ Ca²⁺; ↑ TRPV1-dependent mitochondrial apoptosis Context-dependent P/R Apoptotic amplification Particularly evident with cisplatin; Ca²⁺ has also been implicated in ALA-induced lung-cancer apoptosis.
6 Bax Bcl-2 caspase axis ↑ Bax; ↓ Bcl-2/Bcl-XL; ↑ caspase-3/9; ↑ PARP cleavage Often ↓ inappropriate apoptosis during oxidative injury R/G Apoptosis Downstream convergence point for multiple ALA-responsive pathways.
7 KEAP1 NRF2 p62 ↓ NRF2/p62 in selected prostate models ↑ NRF2; ↑ HO-1/SOD antioxidant defense R/G Context-dependent redox regulation NRF2 should not be classified simply as increased or decreased. ALA activates protective NRF2 signaling in normal cells but can suppress NRF2 in some malignant cells.
8 Glutathione redox system ↑ GSH in some models; ↓ functional antioxidant defense during pro-oxidant killing (context-dependent) ↑ GSH; ↑ GSH/GSSG ratio; ↑ antioxidant protection R/G Redox buffering and context-dependent modulation of apoptosis ALA/DHLA can increase intracellular GSH and stimulate GSH synthesis, particularly in normal or oxidatively stressed cells. In cancer cells, however, increased GSH can oppose ROS-dependent ALA cytotoxicity; several anticancer models instead show ROS accumulation or suppression of antioxidant enzymes. Therefore GSH is mechanistically important but not uniformly anticancer.
9 Autophagy mTOR Beclin-1 LC3 ↓ Beclin-1; ↓ LC3; ↓ autophagy in prostate models Context-dependent G Reduced cancer-cell survival ALA-associated ↑ mTOR and inhibition of autophagy have been reported in LNCaP and DU-145 cells; not established as universal.
10 NF-κB IKK inflammatory signaling ↓ NF-κB (model-dependent) ↓ inflammatory NF-κB activation R/G Reduced survival and inflammatory signaling ALA can inhibit IKK/NF-κB independently of its antioxidant activity, but much of the evidence is from non-malignant experimental systems.
11 Integrin FAK EMT invasion ↓ β1-integrin/FAK; ↓ MMP-2/MMP-9; ↓ EMT Not established G Reduced migration and invasion Preclinical evidence supports antimetastatic effects, but systemic clinical relevance has not been established.
12 Chemosensitization ↑ cisplatin-associated ROS, Ca²⁺ and apoptosis (model-dependent) ↓ chemotherapy-associated oxidative injury in several normal tissues R/G Potential selective treatment modulation ALA can enhance cisplatin cytotoxicity in cultured cancer cells while protecting normal tissue in other models. Clinical net effect on antitumor efficacy is unresolved.
13 Radiosensitivity and radioprotection ↔ antitumor radiosensitization not established ↓ radiation-induced ROS and tissue injury R/G Predominantly radioprotection Human and preclinical literature is oriented toward mitigation of normal-tissue radiation toxicity rather than tumor radiosensitization.
14 Clinical Translation Constraint Common experimental concentrations exceed oral systemic exposure Systemic antioxidant effects occur at clinically used doses G Limits direct anticancer translation Oral bioavailability is approximately 30%, elimination is rapid, and many cancer experiments use 250–1000 µM compared with transient human plasma concentrations typically in the low tens of micromolar.

P: 0–30 min    R: 30 min–3 hr    G: >3 hr

Lipoic acid and Alzheimer’s disease — ALA has sufficient AD-specific mechanistic and human evidence to justify a separate database section, although efficacy remains unproven. Its rationale includes mitochondrial cofactor activity, reduction of oxidative stress, regeneration of endogenous antioxidants, modulation of inflammatory signaling and potential improvement of neuronal glucose/energy metabolism. Small open-label studies using 600 mg/day reported slower cognitive decline, while a small randomized trial of omega-3 plus 600 mg/day ALA found less decline in selected MMSE and instrumental-ADL outcomes but no benefit in its primary oxidative-stress endpoint or ADAS-cog. Another randomized antioxidant combination containing 900 mg/day ALA produced an unexpected greater MMSE decline, making the clinical evidence mixed and insufficient for therapeutic conclusions.

Clinical evidence status: Small human / pilot RCT / adjunct use. No adequately powered confirmatory trial establishes ALA as a disease-modifying treatment for Alzheimer’s disease.

Lipoic Acid in Alzheimer’s Disease

Rank Pathway / Axis Modulation Primary Effect Notes / Interpretation
1 Oxidative stress and glutathione redox cycling ↓ ROS; ↑ antioxidant capacity Neuroprotection ALA/DHLA can scavenge oxidants and regenerate endogenous antioxidant systems; biologically plausible but clinical disease modification is unproven.
2 Mitochondrial energy metabolism ↑ mitochondrial cofactor function Support of neuronal bioenergetics Lipoyl groups are essential cofactors for pyruvate and α-ketoglutarate dehydrogenase complexes.
3 NRF2 antioxidant response ↑ NRF2-associated antioxidant defense Reduced oxidative injury Well supported mechanistically in non-cancer tissues but direct AD clinical validation is limited.
4 NF-κB inflammatory signaling ↓ NF-κB Reduced neuroinflammatory signaling Mechanistically plausible; much supporting evidence is indirect rather than from human AD brain studies.
5 Cognitive and functional decline ↔/↓ decline (study-dependent) Possible clinical neuroprotection Small open-label and omega-3 plus ALA studies produced signals of benefit, but larger confirmatory evidence is lacking and antioxidant-combination data include a possible adverse cognitive signal.


Hif1a, HIF1α/HIF1a: Click to Expand ⟱
Source:
Type:
Hypoxia-Inducible-Factor 1A (HIF1A gene, HIF1α, HIF-1α protein product)
-Dominantly expressed under hypoxia(low oxygen levels) in solid tumor cells
-HIF1A induces the expression of vascular endothelial growth factor (VEGF)
-High HIF-1α expression is associated with Poor prognosis
-Low HIF-1α expression is associated with Better prognosis

-Functionally, HIF-1α is reported to regulate glycolysis, whilst HIF-2α regulates genes associated with lipoprotein metabolism.
-Cancer cells produce HIF in response to hypoxia in order to generate more VEGF that promote angiogenesis

Key mediators of aerobic glycolysis regulated by HIF-1α.
-GLUT-1 → regulation of the flux of glucose into cells.
-HK2 → catalysis of the first step of glucose metabolism.
-PKM2 → regulation of rate-limiting step of glycolysis.
-Phosphorylation of PDH complex by PDK → blockage of OXPHOS and promotion of aerobic glycolysis.
-LDH (LDHA): Rapid ATP production, conversion of pyruvate to lactate;

HIF-1α Inhibitors:
-Curcumin: disruption of signaling pathways that stabilize HIF-1α (ie downregulate).
-Resveratrol: downregulate HIF-1α protein accumulation under hypoxic conditions.
-EGCG: modulation of upstream signaling pathways, leading to decreased HIF-1α activity.
-Emodin: reduce HIF-1α expression. (under hypoxia).
-Apigenin: inhibit HIF-1α accumulation.
Scientific Papers found: Click to Expand⟱
3442- ALA,    α‑lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B - in-vitro, Nor, 3T3
tumCV↓, Notably, α‑LA treatment significantly reduced the cell viability, migration, and invasion of PCa cell lines in a dose‑dependent manner.
TumCMig↓,
TumCI↓,
ROS↑, α‑LA supplementation dramatically increased reactive oxygen species (ROS) levels and HIF‑1α expression, which started the downstream molecular cascade and activated JNK/caspase‑3 signaling pathway
Hif1a↑, The expression of HIF-1α significantly increased following α-LA treatment and was comparable with the changes in ROS.
JNK↑,
Casp↑,
TumCCA↑, arrest of the cell cycle in the S‑phase, which has led to apoptosis of PCa cells
Apoptosis↑,
selectivity↑, Also, the treatment of α‑LA improved bone health by reducing PCa‑mediated bone cell modulation.

3441- ALA,    α-Lipoic Acid Maintains Brain Glucose Metabolism via BDNF/TrkB/HIF-1α Signaling Pathway in P301S Mice
- in-vivo, AD, NA
*tau↓, α-lipoic acid (LA), which is a naturally occurring cofactor in mitochondrial, has been shown to have properties that can inhibit the tau pathology and neuronal damage in our previous research
*GlucoseCon↑, chronic LA administration significantly increased glucose availability by elevating glucose transporter 3 (GLUT3), GLUT4, vascular endothelial growth factor (VEGF) protein and mRNA level, and heme oxygenase-1 (HO-1) protein level in P301S mouse brain
*GLUT3↑,
*GLUT4↑,
*VEGF↑,
*HO-1↑,
*Glycolysis↑, LA also promoted glycolysis by directly upregulating hexokinase (HK) activity, indirectly by increasing proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and DNA repair enzymes (OGG1/2 and MTH1).
*HK1↑, Our results indicated that the activity of HK was significantly increased after 10 mg/kg LA treatment.
*PGC-1α↑,
*Hif1a↑, found the underlying mechanism of restored glucose metabolism might involve in the activation of brain-derived neurotrophic factor (BDNF)/tyrosine Kinase receptor B (TrkB)/hypoxia-inducible factor-1α (HIF-1α) signaling pathway by LA treatment.
*neuroP↑,

3433- ALA,    Alpha lipoic acid promotes development of hematopoietic progenitors derived from human embryonic stem cells by antagonizing ROS signals
*ROS↓, However, in more mature hPSC‐derived hematopoietic stem/progenitor cells, ALA reduced ROS levels and inhibited apoptosis.
*Apoptosis↓,
*Hif1a↑, up‐regulating HIF1A in response to a hypoxic environment.
*FOXO1↑, ALA also up‐regulated sensor genes of ROS signals, including HIF1A, FOXO1, FOXO3, ATM, PETEN, SIRT1, and SIRT3, during the process of hPSCs derived hemogenic endothelial cells generation
*FOXO3↑,
*ATM↑,
*SIRT1↑,
*SIRT3↑,
*CD34↑, Flow cytometry analysis indicated that ALA improved the production of CD34+ CD43+ CD45+ hematopoietic stem/progenitor cells significantly

3271- ALA,    Decrypting the potential role of α-lipoic acid in Alzheimer's disease
- Review, AD, NA
*antiOx↑, Alpha-lipoic acid (α-LA), a natural antioxidant
*memory↑, multiple preclinical studies indicating beneficial effects of α-LA in memory functioning, and pointing to its neuroprotective effects
*neuroP↑, α-LA could be considered neuroprotective
*Inflam↓, α-LA shows antioxidant, antiapoptotic, anti-inflammatory, glioprotective, metal chelating properties in both in vivo and in vitro studies.
*IronCh↑, α-LA leads to a marked downregulation in iron absorption and active iron reserve inside the neuron
*NRF2↑, α-LA induces the activity of the nuclear factor erythroid-2-related factor (Nrf2), a transcription factor.
*BBB↑, capable of penetrating the BBB
*GlucoseCon↑, Fig 2, α-LA mediated regulation of glucose uptake
*Ach↑, α-LA may show its action on the activity of the ChAT enzyme, which is an essential enzyme in acetylcholine metabolism
*ROS↓,
*p‑tau↓, decreased degree of tau phosphorylation following treatment with α-LA
*Aβ↓, α-LA possibly induce the solubilization of Aß plaques in the frontal cortex
*cognitive↑, cognitive reservation of α-LA served AD model was markedly upgraded in additional review
*Hif1a↑, α-LA treatment efficaciously induces the translocation and activity of hypoxia-inducible factor-1α (HIF-1α),
*Ca+2↓, research found that α-LA therapy remarkably declines Ca2+ concentration and calpain signaling
*GLUT3↑, inducing the downstream target genes expression, such as GLUT3, GLUT4, HO-1, and VEGF.
*GLUT4↑,
*HO-1↑,
*VEGF↑,
*PDKs↓, α-LA also ameliorates survival in mutant mice of Huntington's disease [150–151], possibly due to the inhibition of the activity of pyruvate dehydrogenase kinase
*PDH↑, α-LA administration enhances PDH expression in mitochondrial hepatocytes by inhibiting the pyruvate dehydrogenase kinase (PDK),
*VCAM-1↓, α-LA inhibits the expression of cell-cell adhesion molecule-1 and VCAM-1 in spinal cords and TNF-α induced neuronal endothelial cells injury
*GSH↑, α-LA may enhance glutathione production in old-aged models
*NRF2↑, activation of the Nrf2 signaling by α-LA
*hepatoP↑, α-LA also protected the liver against oxidative stress-mediated hepatotoxicity
*ChAT↑, α-LA in mice models may prevent neuronal injury possibly due to an increase in ChAT in the hippocampus of animal models

278- ALA,    The Multifaceted Role of Alpha-Lipoic Acid in Cancer Prevention, Occurrence, and Treatment
- Review, NA, NA
ROS↑, direct anticancer effect of the antioxidant ALA is manifested as an increase in intracellular ROS levels in cancer cells
NRF2↑, enhance the activity of the anti-inflammatory protein nuclear factor erythroid 2–related factor 2 (Nrf2), thereby reducing tissue damage
Inflam↓,
frataxin↑,
*BioAv↓, Oral ALA has a bioavailability of approximately 30% due to issues such as poor stability in the stomach, low solubility, and hepatic degradation.
ChemoSen↑, ALA can enhance the functionality of various other anticancer drugs, including 5-fluorouracil in colon cancer cells and cisplatin in MCF-7 breast cancer cells
Hif1a↓, it is inferred that lipoic acid may inhibit the expression of HIF-1α
eff↑, act as a synergistic agent with natural polyphenolic substances such as apigenin and genistein
FAK↓, ALA inhibits FAK activation by downregulating β1-integrin expression and reduces the levels of MMP-9 and MMP-2
ITGB1↓,
MMP2↓,
MMP9↓,
EMT↓, ALA inhibits the expression of EMT markers, including Snail, vimentin, and Zeb1
Snail↓,
Vim↓,
Zeb1↓,
P53↑, ALA also stimulates the mutant p53 protein and depletes MGMT
MGMT↓, depletes MGMT by inhibiting NF-κB signalling, thereby inducing apoptosis
Mcl-1↓,
Bcl-xL↓,
Bcl-2↓,
survivin↓,
Casp3↑,
Casp9↑,
BAX↑,
p‑Akt↓, ALA inhibits the activation of tumour stem cells by reducing Akt phosphorylation.
GSK‐3β↓, phosphorylation and inactivation of GSK3β
*antiOx↑, indirect antioxidant protection through metal chelation (ALA primarily binds Cu2+ and Zn2+, while DHLA can bind Cu2+, Zn2+, Pb2+, Hg2+, and Fe3+) and the regeneration of certain endogenous antioxidants, such as vitamin E, vitamin C, and glutathione
*ROS↓, ALA can directly quench various reactive species, including ROS, reactive nitrogen species, hydroxyl radicals (HO•), hypochlorous acid (HclO), and singlet oxygen (1O2);
selectivity↑, In normal cells, ALA acts as an antioxidant by clearing ROS. However, in cancer cells, it can exert pro-oxidative effects, inducing pathways that restrict cancer progression.
angioG↓, Combining these two hypotheses, it can be hypothesized that ALA may regulate copper and HIF-2α to limit tumor angiogenesis.
MMPs↓, ALA was shown to inhibit invasion by decreasing the mRNA levels of key matrix metalloproteinases (MMPs), specifically MMP2 and MMP9, which are crucial for the metastatic process
NF-kB↓, ALA has been shown to enhance the efficacy of the chemotherapeutic drug paclitaxel in breast and lung cancer cells by inhibiting the NF-κB signalling pathway and the functions of integrin β1/β3 [138,139]
ITGB3↓,
NADPH↓, ALA has been shown to inhibit NADPH oxidase, a key enzyme closely associated with NP, including NOX4

277- ALA,    α-lipoic acid modulates prostate cancer cell growth and bone cell differentiation
- in-vitro, Pca, 22Rv1 - in-vitro, Pca, C4-2B
ROS↑, α-LA supplementation dramatically increased reactive oxygen species (ROS) levels and HIF-1α expression, which started the downstream molecular cascade and activated JNK/caspase-3 signaling pathway.
Hif1a↑, HIF-1α, is a key regulator in response to cellular stressors, and excessive ROS levels can influence its expression. (HIF-1α) is essential for the physiological response to hypoxia(resulting from elevated intracellular ROS levels)
JNK↑,
Casp3↑,
P21↑,
BAX↑,
Bcl-xL↓,
cFos↓,


Showing Research Papers: 1 to 6 of 6

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 6

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

frataxin↑, 1,   NRF2↑, 1,   ROS↑, 3,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

NADPH↓, 1,  

Cell Death(tgid=5) ⓘ

p‑Akt↓, 1,   Apoptosis↑, 1,   BAX↑, 2,   Bcl-2↓, 1,   Bcl-xL↓, 2,   Casp↑, 1,   Casp3↑, 2,   Casp9↑, 1,   JNK↑, 2,   Mcl-1↓, 1,   survivin↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

tumCV↓, 1,  

DNA Damage & Repair(tgid=10) ⓘ

MGMT↓, 1,   P53↑, 1,  

Cell Cycle & Senescence(tgid=11) ⓘ

P21↑, 1,   TumCCA↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

cFos↓, 1,   EMT↓, 1,   GSK‐3β↓, 1,  

Migration(tgid=13) ⓘ

FAK↓, 1,   ITGB1↓, 1,   ITGB3↓, 1,   MMP2↓, 1,   MMP9↓, 1,   MMPs↓, 1,   Snail↓, 1,   TumCI↓, 1,   TumCMig↓, 1,   Vim↓, 1,   Zeb1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

angioG↓, 1,   Hif1a↓, 1,   Hif1a↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,   NF-kB↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

ChemoSen↑, 1,   eff↑, 1,   selectivity↑, 2,  
Total Targets: 42

Pathway results for Effect on Normal Cells:


Redox & Oxidative Stress(tgid=1) ⓘ

antiOx↑, 2,   GSH↑, 1,   HK1↑, 1,   HO-1↑, 2,   NRF2↑, 2,   ROS↓, 3,   SIRT3↑, 1,  

Metal & Cofactor Biology(tgid=2) ⓘ

IronCh↑, 1,  

Mitochondria & Bioenergetics(tgid=3) ⓘ

PGC-1α↑, 1,  

Core Metabolism/Glycolysis(tgid=4) ⓘ

GlucoseCon↑, 2,   Glycolysis↑, 1,   PDH↑, 1,   PDKs↓, 1,   SIRT1↑, 1,  

Cell Death(tgid=5) ⓘ

Apoptosis↓, 1,  

Transcription & Epigenetics(tgid=7) ⓘ

Ach↑, 1,  

DNA Damage & Repair(tgid=10) ⓘ

ATM↑, 1,  

Proliferation, Differentiation & Cell State(tgid=12) ⓘ

CD34↑, 1,   FOXO1↑, 1,   FOXO3↑, 1,  

Migration(tgid=13) ⓘ

Ca+2↓, 1,   VCAM-1↓, 1,  

Angiogenesis & Vasculature(tgid=14) ⓘ

Hif1a↑, 3,   VEGF↑, 2,  

Barriers & Transport(tgid=15) ⓘ

BBB↑, 1,   GLUT3↑, 2,   GLUT4↑, 2,  

Immune & Inflammatory Signaling(tgid=16) ⓘ

Inflam↓, 1,  

Synaptic & Neurotransmission(tgid=18) ⓘ

ChAT↑, 1,   tau↓, 1,   p‑tau↓, 1,  

Protein Aggregation(tgid=19) ⓘ

Aβ↓, 1,  

Drug Metabolism & Resistance(tgid=21) ⓘ

BioAv↓, 1,  

Functional Outcomes(tgid=23) ⓘ

cognitive↑, 1,   hepatoP↑, 1,   memory↑, 1,   neuroP↑, 2,  
Total Targets: 37

Scientific Paper Hit Count for: Hif1a, HIF1α/HIF1a
6 Alpha-Lipoic-Acid
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#:29  Target#:143  State#:%  Dir#:%
  wNotes=on  sortOrder:rid,rpid

 

Home Page