OPA1 Cancer Research Results

OPA1, Optic Atrophy 1: Click to Expand ⟱
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Type:

MFN1, MFN2, and OPA1 are mostly AD / neurodegeneration-relevant pathway targets: In AD, the general pattern is: fusion proteins MFN1, MFN2, and OPA1 tend to be reduced or functionally impaired, while fission signaling such as DRP1/FIS1 is often increased, contributing to fragmented mitochondria, synaptic injury, oxidative stress, and impaired bioenergetics

MFN1, MFN2, and OPA1 are mitochondrial fusion regulators. MFN1 and MFN2 mediate outer mitochondrial membrane fusion, while OPA1 mediates inner mitochondrial membrane fusion and helps maintain cristae structure. In Alzheimer’s disease and related neurodegenerative models, mitochondrial dynamics are commonly shifted toward excessive fragmentation, with reduced or impaired fusion signaling and increased fission stress. Restoring MFN2/OPA1/MFN1 activity may help preserve mitochondrial network integrity, oxidative phosphorylation, neuronal transport, calcium handling, and synaptic resilience.

Target / Pathway Primary Disease Relevance Normal Function Observed / Suspected Change in AD Therapeutic Direction Database Interpretation Evidence Strength Notes for Product Screening
MFN1 Mostly AD / neurodegeneration; secondary cancer relevance Outer mitochondrial membrane fusion protein. Works with MFN2 to tether and fuse adjacent mitochondria, helping maintain mitochondrial network integrity and mitochondrial DNA/protein complementation. Generally reported as reduced or functionally impaired in AD-related mitochondrial dynamics imbalance, contributing to mitochondrial fragmentation and reduced neuronal bioenergetic resilience. Support / restore mitochondrial fusion where excessive fission and mitochondrial fragmentation are present. Pathway target rather than product. Useful as part of a broader “mitochondrial fusion support” or “anti-fragmentation” pathway entry. Moderate Track products that increase MFN1 expression, improve mitochondrial network morphology, reduce DRP1-driven fragmentation, or restore fusion/fission balance.
MFN2 Strong AD / neurodegeneration relevance; also cancer and metabolic relevance Outer mitochondrial membrane fusion protein. Also involved in mitochondria-ER contact regulation, calcium handling, mitophagy-related quality control, mitochondrial trafficking, and cellular stress adaptation. MFN2 dysfunction or downregulation is associated with impaired mitochondrial fusion, abnormal mitochondria-ER communication, calcium stress, oxidative stress, synaptic vulnerability, and possibly amyloid/tau-associated mitochondrial injury. Usually upmodulation / restoration is desirable in AD models where mitochondrial fragmentation, poor transport, or excessive fission is present. High-priority AD target. Best entered as a mitochondrial dynamics, fusion, ER-mitochondria contact, and mitophagy-quality-control target. Moderate-Strong Track products that increase MFN2, improve mitochondrial elongation, reduce Aβ/tau-induced mitochondrial fragmentation, improve calcium homeostasis, or restore mitochondrial transport in neurons.
OPA1 Strong AD / neurodegeneration relevance; also apoptosis and cancer relevance Inner mitochondrial membrane fusion protein. Maintains cristae structure, supports oxidative phosphorylation, preserves mitochondrial membrane organization, and helps regulate cytochrome-c release during apoptosis. OPA1 loss or cleavage can reduce inner membrane fusion, destabilize cristae, impair oxidative phosphorylation, increase mitochondrial fragmentation, and sensitize neurons to synaptic and metabolic stress. Support / stabilize OPA1 activity, especially long-form fusion-active OPA1, where mitochondrial stress causes excessive OPA1 cleavage and fragmentation. High-priority AD target. Best entered under mitochondrial fusion, cristae integrity, oxidative phosphorylation, and apoptosis-resistance pathways. Moderate-Strong Track products that preserve OPA1, reduce pathological OPA1 cleavage, improve cristae integrity, improve ATP production, or reduce mitochondrial apoptosis signaling.


Scientific Papers found: Click to Expand⟱
6416- CUR,  QC,  FA,  RES,  EGCG  Natural products targeting mitochondria: emerging therapeutics for age-associated neurological disorders
- Review, AD, NA
*DRP1/DNM1L↓, Resveratrol was shown to regulate mitochondrial fusion/fission dynamics through increasing the expression of MFN2 and OPA1 while decreasing the expression of DRP1 and FIS1
*FIS1↓,
*MFN2↑, Resveratrol also increased OPA1 and MFN2 expression to promote mitochondrial fusion in the hippocampus of SAMP8 mice, a model of dementia
*OPA1↑,
*DRP1/DNM1L↓, curcumin can reduce mitochondrial fission by decreasing the expression of DRP1 and FIS1, and enhance fusion by increasing the expression of OPA1, MFN1 and MFN2 in the brains of SAMP8 mice
*FIS1↓,
*OPA1↑,
*MFN1↑,
*MFN2↑,
*DRP1/DNM1L↓, quercetin was found to regulate mitochondrial dynamics by inhibiting the expression of DRP1 and FIS1 and at the same time increasing the expression of MFN1 and MFN2 in the rat hippocampus, thereby improving hypoxia-induced memory deficits
*FIS1↓,
*MFN1↑,
*MFN2↑,
*memory↑,
*mtDam↓, EGCG was found to protect mitochondrial function by down-regulating the expression of DRP1 and FIS1 in the brain
*DRP1/DNM1L↓,
*FIS1↓,

6419- MEL,    The potential influence of melatonin on mitochondrial quality control: a review
- Review, Nor, NA
*mt-ACC⇅, Melatonin regulates pyruvate or fatty acid metabolism to increase the concentration of acetyl-CoA in mitochondria. these studies indicate that melatonin increases or decreases acetyl-CoA content in mitochondria to regulate mitochondrial metabolism.
*PKM1↑, melatonin increases the activity of pyruvate kinase M1/2 (PKM) to regulate glycolysis
*PKM2↑,
*Glycolysis↝,
*PDKs↑, melatonin activates pyruvate dehydrogenase kinase 4 (PDK4) to regulate acetyl-CoA content
*FAO↑, melatonin can promote fatty acid metabolism by directly enhancing β-oxidation or increasing the transfer of fatty acid-derived acetyl-CoA into mitochondria
*ETC↑, Second, melatonin can enhance the activity of the electron-transport chain (ETC) and oxidative phosphorylation (OXPHOS) to regulate mitochondrial metabolism.
*OXPHOS↑,
*ATP↑, melatonin enhanced OXPHOS and promoted adenosine triphosphate (ATP) synthesis in rat brain and liver mitochondria
Glycolysis↓, ome studies have found that melatonin drove the switch from cytosolic glycolysis to mitochondrial OXPHOS in cancer cells
OXPHOS↑,
*Ca+2↓, melatonin can regulate the membrane potential of mitochondria and decrease excessive calcium levels to enhance ETC activity to increase ATP production
*ROS↓, Melatonin exhibits superior antioxidant ability. Melatonin, as a major scavenger of reactive oxygen species (ROS), may play a pivotal role in protecting mitochondria from ROS-induced injury
*antiOx↑, These specific characteristics make melatonin a broad-spectrum antioxidant.
*SOD2↑, melatonin can upregulate the expression of superoxide dismutase (MnSOD), glutathione peroxidase (GSH-Px) and catalase (CAT) to prevent cell stress and injury
*GPx↑,
*Catalase↑,
*MFN1↑, On the one hand, melatonin increases mitochondrial fusion-related genes such as mitofusin-1 (Mfn1), mitofusin-2 (Mfn2) and optic atrophy1 (Opa1) to promote mitochondrial fusion
*MFN2↑,
*OPA1↑,
*YAP/TEAD↑, studies have found that melatonin activated the Yap-Hippo pathway to increase Opa1-related fusion
*Hippo↑,
*SIRT1↑, melatonin alleviated cardiac dysfunction induced by diabetes by upregulating SIRT1-PGC1α to inhibit the expression of Drp1
*PGC-1α↑,
*DRP1/DNM1L↓,

6420- RES,    Resveratrol Regulates Mitochondrial Biogenesis and Fission/Fusion to Attenuate Rotenone-Induced Neurotoxicity
- in-vivo, Park, NA
*DRP1/DNM1L↑, resveratrol pretreatment could improve the ability of mitochondrial fission and fusion, by promoting expression of Drp1, Fis1, OPA1, and MFN2 mRNA and protein associated with mitochondrial fission and fusion
*FIS1↑,
*OPA1↑,
*MFN2↑,
*motorD↑, resveratrol pretreatment decreased the disturbance of motor coordination, with the rate and duration of motion enhanced significantly.
*PGC-1α↑, Moreover, resveratrol pretreatment could reverse the inhibition of PGC-1α and mtTFA protein and mRNA expression caused by rotenone
*ROS↓, if PC12 cells were pretreated with resveratrol, the ROS production decreased (Figure 5(a)) and ATP production (Figure 5(b)) increased significantly
*ATP↑,


Showing Research Papers: 1 to 3 of 3

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 3

Pathway results for Effect on Cancer / Diseased Cells:


Redox & Oxidative Stress ⓘ

OXPHOS↑, 1,  

Core Metabolism/Glycolysis ⓘ

Glycolysis↓, 1,  
Total Targets: 2

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

DRP1/DNM1L↓, 5,   DRP1/DNM1L↑, 1,   FIS1↓, 4,   FIS1↑, 1,   MFN1↑, 3,   MFN2↑, 5,   OPA1↑, 4,  

Redox & Oxidative Stress ⓘ

antiOx↑, 1,   Catalase↑, 1,   GPx↑, 1,   OXPHOS↑, 1,   ROS↓, 2,   SOD2↑, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 2,   ETC↑, 1,   mtDam↓, 1,   PGC-1α↑, 2,  

Core Metabolism/Glycolysis ⓘ

mt-ACC⇅, 1,   FAO↑, 1,   Glycolysis↝, 1,   PDKs↑, 1,   PKM1↑, 1,   PKM2↑, 1,   SIRT1↑, 1,  

Cell Death ⓘ

Hippo↑, 1,   YAP/TEAD↑, 1,  

Migration ⓘ

Ca+2↓, 1,  

Functional Outcomes ⓘ

memory↑, 1,   motorD↑, 1,  
Total Targets: 29

Scientific Paper Hit Count for: OPA1, Optic Atrophy 1
2 Resveratrol
1 Curcumin
1 Quercetin
1 Ferulic acid
1 EGCG (Epigallocatechin Gallate)
1 Melatonin
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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