🧫
Gap26 inhibitor treatment in cellular TMJOA model
active
experiment
Created: 2026-04-10T22:49:52
By: etl-v1-backfill
Quality:
50%
✓ SciDEX
ID: exp-dd170ed1-e7d7-41dc-ba80-5cd1453be1e2
🧫 Experiment Protocol
ExploratoryTemporomandibular joint osteoarthritisCx43H₂O₂-treated chondrocytes with Gap26 inhibitorproposed
A pharmacological intervention study using Gap26, a specific Connexin 43 inhibitor, to investigate the functional role of Cx43 in chondrocyte responses to oxidative stress. The study examined whether blocking Cx43 hemichannel function could prevent or reduce oxidative stress-induced degenerative changes, Wnt/β-catenin signaling activation, and extracellular matrix degradation in the cellular model of TMJOA.
PRIMARY OUTCOME
Reduced hemichannel opening and suppressed Wnt signaling
EXPECTED OUTCOMES
Gap26 would reduce hemichannel opening, suppress Wnt signaling, and mitigate degenerative changes
SUCCESS CRITERIA
Demonstration of reduced hemichannel activity, decreased Wnt/β-catenin signaling, and protection against degenerative changes
PROTOCOL
Treatment of chondrocytes with Gap26 inhibitor followed by H₂O₂-induced oxidative stress, assessment of hemichannel function, Wnt/β-catenin signaling, and degenerative markers
Source: PMID 41757775 ↗
🧫 Experiment Extras
PATHWAY
Wnt/β-catenin signaling
MARKET PRICE
$0.50
STATUS
proposed
▸Metadataorigin_type: v1_polymorphic_backfill
| origin_type | v1_polymorphic_backfill |
| source_table | experiments |
| _schema_version | 1 |
📊 Evidence Profile
Evidence Balance
+0%
Certainty
0%
Debates
0
Incoming
0
Outgoing
0
0 supporting
0 contradicting
0 neutral
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