TL;DR
METTL1 aggravated myocardial injury by inhibiting PINK1/Parkin-mediated mitophagy through the upregulation of USF2 in a m7G-dependent manner in SCM models, thereby identifying METTL1 as a potential therapeutic target for SCM.
These findings identify the PGAM5/VDAC1 axis as a key mechanism linking ponatinib stress to coordinated failure of MQC in the heart and targeting PGAM5-dependent VDAC1 oligomerization may represent a potential strategy for limiting ponatinib-associated cardiotoxicity.
ZNF143 upregulation exacerbated MASLD progression by mediating TRPV1 ubiquitination and degradation through transcriptionally activating SMURF1, and its knockdown mitigated lipid accumulation and liver injury by activating hepatocyte mitophagy.
It is demonstrated that the methylation level is highly expressed in the septic liver injury, complying with the up-regulation of m6A methyltransferase METTL4 and the reader YTHDF1, and provides a potential therapeutic target to treat sepsis-induced liver injury.
Results demonstrate that SREBF2 mitigates MI-induced HF by activating the Cav-1/PINK1/Parkin axis to promote mitophagy and inhibit ferroptosis, and identify SREBF2 as a promising therapeutic target in heart failure.
BACKGROUND Myocardial ischemia/reperfusion (MI/R) injury remains a major clinical challenge characterized by inflammation and progressive cardiomyocyte loss. Although pyroptosis is known to drive this pathogenesis, the upstream molecular switches that trigger the pyroptotic cascade remain poorly understood. Here, we in...
Background: Sepsis-induced acute lung injury (ALI) is a critical clinical challenge with substantial mortality. While mitophagy plays a pivotal role in ALI pathogenesis, the mechanisms underlying the involvement of nuclear receptor binding factor 2 (NRBF2), a key regulator of autophagy, in this process remain unexplore...
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