First-pass extracted concept

p62/SQSTM1

Candidate: concept label1 source documents7 linked claims

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Aliases

p62, SQSTM1

Evidence Snippets

To define the role of the autophagy hub protein p62/SQSTM1 in I/R injury...

Evidence 1Source 1DOI PubMedprovenance

Supporting Sources

Source 1primary paper2025MEDDOI PubMed

1 evidence snippet 7 linked claims Claim 1 Claim 2 Claim 3

Linked Claims

Claim 1causal effectsupports2025Source 1DOI PubMed

p62 overexpression increases ischemia/reperfusion injury, whereas p62 knockdown or pharmacological deactivation reduces injury.

Claim 2disease relevancesupports2025Source 1DOI PubMed

The study establishes p62 as a master regulator of ischemia/reperfusion injury and a potential target for stroke therapies.

Claim 3expression changesupports2025Source 1DOI PubMed

p62 levels increase after ischemia/reperfusion and track with intracellular ROS changes.

Claim 4mechanismsupports2025Source 1DOI PubMed

The death-promoting effects of p62 involve elevated ROS burden.

Claim 5mechanistic dependencysupports2025Source 1DOI PubMed

Autophagic flux is p62-dependent but oxygen-independent in the reported ischemia/reperfusion context.

Claim 6pathway regulationsupports2025Source 1DOI PubMed

p62 activates NRF2-associated antioxidant signaling and inhibits the pro-inflammatory NFκB pathway, with bidirectional linkage between these responses and p62.

Claim 7pathway regulationsupports2025Source 1DOI PubMed

p62 downregulates BiP/GRP78 and consecutively activates the UPR PERK branch in the reported ischemia/reperfusion context.