OPA1 Cancer Research Results

OPA1, Optic Atrophy 1: Click to Expand ⟱
Source:
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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⟱
6422- QC,    Quercetin Protects Ethanol-Induced Hepatocyte Pyroptosis via Scavenging Mitochondrial ROS and Promoting PGC-1α-Regulated Mitochondrial Homeostasis in L02 Cells
- in-vitro, Alcohol, L02
*mt-ROS↓, *lipid-P↓, *MMP↑, *mtDam↓, *NLRP3↓, *ASC↓, *cl‑Casp1↓, *IL18↓, *IL1β↓, *GSDMD↓, *Pyro↓, *CYP2E1↓, *MFN1↓, *MFN2↓, *OPA1↓, *DRP1/DNM1L↑,
6423- RES,    Resveratrol Regulates Mitochondrial Biogenesis and Fission/Fusion to Attenuate Rotenone-Induced Neurotoxicity
- vitro+vivo, Park, NA
*neuroP↑, *FIS1↓, *OPA1↓, *MFN2↓, *PGC-1α↑, *ROS↓, *ATP↑, *motorD↑,

Showing Research Papers: 1 to 2 of 2

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 2

Pathway results for Effect on Cancer / Diseased Cells:


Total Targets: 0

Pathway results for Effect on Normal Cells:


NA, unassigned ⓘ

DRP1/DNM1L↑, 1,   FIS1↓, 1,   MFN1↓, 1,   MFN2↓, 2,   OPA1↓, 2,  

Redox & Oxidative Stress ⓘ

CYP2E1↓, 1,   lipid-P↓, 1,   ROS↓, 1,   mt-ROS↓, 1,  

Mitochondria & Bioenergetics ⓘ

ATP↑, 1,   MMP↑, 1,   mtDam↓, 1,   PGC-1α↑, 1,  

Cell Death ⓘ

cl‑Casp1↓, 1,   GSDMD↓, 1,   Pyro↓, 1,  

Immune & Inflammatory Signaling ⓘ

ASC↓, 1,   IL18↓, 1,   IL1β↓, 1,  

Protein Aggregation ⓘ

NLRP3↓, 1,  

Functional Outcomes ⓘ

motorD↑, 1,   neuroP↑, 1,  
Total Targets: 22

Scientific Paper Hit Count for: OPA1, Optic Atrophy 1
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#:1491  State#:%  Dir#:1
  wNotes=0  sortOrder:rid,rpid

 

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