What molecular mechanism causes VCP mutations to trigger aberrant HIF-1α activation under normoxic conditions?
Analysis ID: SDA-2026-04-13-gap-pubmed-20260410-170057-1bea7d88 | Domain: neurodegeneration | Status: failed | Created: 2026-04-13T17:25:04.702967
Knowledge Graph: 2 edges — View JSON
Top Hypotheses (2 total)
#1 Targeting SASP-Complement Amplification Through HIF-1α Downstream Effectors
0.610
C1QA, C1QB, C3, IL1B
Blocking the IL-1β/C1Q axis to prevent astrocyte-microglia cross-dysfunction mediated by HIF-1α. The SASP-mediated complement cascade amplification represents a downstream consequence of HIF-1α activa
#2 TFEB Nuclear Translocation to Reset Lysosomal-Hypoxia Axis
0.575
TFEB, MTOR
## Molecular Mechanism and Rationale
This hypothesis proposes that pharmacological activation of TFEB (Transcription Factor EB) nuclear translocation can simultaneously restore lysosomal homeostasis