MitoP Cancer Research Results
MitoP, Mitophagy: Click to Expand ⟱
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Mitophagy—the selective autophagic removal of damaged mitochondria—is now regarded as a core upstream process in Alzheimer’s disease pathophysiology, not a secondary epiphenomenon. Impairment of mitophagy precedes overt amyloid and tau pathology and helps explain early synaptic failure and neuronal vulnerability.
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Scientific Papers found: Click to Expand⟱
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*MitoP↓, Experimental models consistently show that UA increases mitophagy and mitochondrial function and blunts excessive inflammatory responses.
*Strength↑, UA is a promising strategy to target health and disease conditions of aging, especially those linked to mitochondrial and muscle dysfunction.
*PINK1↑, UA can activate. PTEN-induced kinase 1 (PINK1)/Parkin-dependent mitophagy starts with the stabilization of the kinase PINK1,
*PARK2↑, which recruits and phosphorylates the ubiquitin-conjugating protein Parkin.
*Inflam↓, anti-inflammatory effect of UA was reported for the first time as a decrease in mRNA and protein levels of the inflammatory marker cyclooxygenase 2 (COX2)
*COX2↓,
*IL1β↓, In neuronal tissues, UA treatment reduced levels of IL-1β, IL-6, and TNFα in the brains of the amyloid precursor protein/presenilin 1 (APP/PS1) mouse model of AD
*IL6↓,
*TNF-α↓,
*OS↑, impact on worm longevity showed that UA extends lifespan by 45%,
*cardioP↑, reduction in IRI markers, such as circulating creatine kinase and lactate dehydrogenase levels, and by fewer apoptotic cells in the heart
*memory↑, Increased learning, memory retention, neuronal survival, and neurogenesis in the hippocampus was achieved with UA administration in the APP/PS1 mouse model of AD
*neuroG↑,
*neuroP↑, UA was shown to have neuroprotective effects in the EAE mouse model of multiple sclerosis (MS)
*Cartilage↑, In a model of osteoarthritis, an age-related and disabling joint disease caused by a slow degeneration of cartilage,
*Inflam↓, UA has protective effects against a chronic DSS-induced model of IBD, leading to reduced levels of colon inflammation markers and to better mucosal integrity.
*RenoP↑, UA consistently reduced tubular damage induced by cisplatin, as shown by histopathology and by a reduction in circulating markers of kidney damage
*eff↑, When administered as nanoparticles to increase its bioavailability, UA even improved the survival of mice that received a lethal dose of cisplatin
*Dose↝, UA showed a favorable safety profile, with no observed side effects following either single oral administration of UA up to 2000 mg or multiple oral dosing (28 days) of UA up to 1000 mg daily.
*Half-Life↑, It showed a relatively long-half life (t1/2 = 17–22 hours),
*NRF2↑, Other mechanisms of action have been proposed for UA, such as the activation of the Ahr/Nrf2 pathway and its downstream antioxidative stress response
*GutMicro↑, A recent report also showed an impact of direct UA supplementation on gut microflora in obese rats
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:
Redox & Oxidative Stress ⓘ
NRF2↑, 1, PARK2↑, 1,
Mitochondria & Bioenergetics ⓘ
PINK1↑, 1,
Autophagy & Lysosomes ⓘ
MitoP↓, 1,
Proliferation, Differentiation & Cell State ⓘ
neuroG↑, 1,
Migration ⓘ
Cartilage↑, 1,
Immune & Inflammatory Signaling ⓘ
COX2↓, 1, IL1β↓, 1, IL6↓, 1, Inflam↓, 2, TNF-α↓, 1,
Drug Metabolism & Resistance ⓘ
Dose↝, 1, eff↑, 1, Half-Life↑, 1,
Clinical Biomarkers ⓘ
GutMicro↑, 1, IL6↓, 1,
Functional Outcomes ⓘ
cardioP↑, 1, memory↑, 1, neuroP↑, 1, OS↑, 1, RenoP↑, 1, Strength↑, 1,
Total Targets: 22
Scientific Paper Hit Count for: MitoP, Mitophagy
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
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