Zhang Hong team finds PIEZO1/TRPV1 trigger ER‑phagy
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- Zhang Hong’s team used super‑resolution multi‑SIM live‑cell imaging to show that under stress, Ca²⁺‑rich ER sheet subdomains expand and become engulfed by autophagosomes.
- FAM134B together with lipidated LC3 coordinates autophagosome formation whose membranes derive directly from the remodeled ER.
- PIEZO1 (and TRPV1) mechanosensitive channels are enriched in Ca²⁺‑rich ER sheets and generate localized Ca²⁺ release signals.
- Ca²⁺ transients induce liquid‑liquid phase separation of the autophagy‑initiating FIP200 complex, initiating ER‑phagy.
- The study was published on April 2, 2026 in Molecular Cell (doi:10.1016/j.molcel.2026.03.002).
- ER‑phagy dysfunction is linked to neurodegenerative disorders and cancer, highlighting new therapeutic targets.
Why it matters: The mechanistic link between PIEZO1/TRPV1‑driven Ca²⁺ bursts and FIP200‑mediated autophagosome initiation gives researchers a concrete molecular target for drugs that restore ER‑phagy, directly addressing the cellular dysfunction implicated in neurodegenerative disease and cancer, providing a pathway to develop interventions for these diseases.
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