MARCH7 identified as key regulator suppressing ferroptosis through iron homeostasis control
By
Junbing Wu7 Send email to [email protected]
Plain bagel done well. Pleasantly substantive.
Summary
This article identifies the E3 ubiquitin ligase MARCH7 as a critical regulator that suppresses ferroptosis (an iron-dependent form of regulated cell death) by controlling intracellular iron homeostasis. Through multi-omics analysis, researchers found that MARCH7 ubiquitylates NCOA4, promoting its degradation and reducing the labile iron pool. The study also identifies a small molecule stabilizer called EmodAn that offers cardioprotection, positioning MARCH7 as a promising therapeutic target for ferroptosis-related diseases.
Key quotes
· 3 pulledMARCH7 ubiquitylates nuclear receptor coactivator 4 (NCOA4) at residue Lys42 by K48-linked ubiquitination, promoting NCOA4 proteasomal degradation and reducing the labile iron pool.
A small molecule stabilizer, EmodAn, offers robust cardioprotection, highlighting MARCH7 as a promising target for treating ferroptosis-related diseases.
Utilizing multi-omics, we identify the E3 ubiquitin ligase membrane-associated RING-CH 7 (MARCH7) as a non-redundant, dual suppressor of ferroptosis via direct regulation of intracellular iron homeostasis.
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