I. Wittig

The aging-induced long non-coding RNA MIRIAL controls endothelial cell and mitochondrial function

This paper identifies MIRIAL as an aging-induced lncRNA that regulates endothelial quiescence and mitochondrial function through a novel triplex mechanism.

Immortalised murine R349P desmin knock-in myotubes exhibit a reduced proton leak and decreased ADP/ATP translocase levels in purified mitochondria

This paper establishes an immortalised murine desminopathy model and finds reduced mitochondrial proton leak and ADP/ATP translocase levels in desminopathy myotubes.

MIC13 and SLP2 seed the assembly of MIC60-subcomplex to facilitate crista junction formation

This study identifies SLP2 as an auxiliary MICOS subunit that interacts with MIC13 to seed MIC60 assembly and promote crista junction formation.

Ena/VASP proteins mediate endothelial cell repulsion from ephrin ligands

This study shows that Ena/VASP proteins are essential for endothelial cell repulsion from ephrin-B2 by mediating actin cytoskeleton collapse and Eph receptor signaling.

The lncRNA landscape of cardiac resident macrophages and identification of Schlafenlnc as a regulator of macrophage migratory function

The paper identifies lncRNAs in cardiac resident macrophages and shows Schlafenlnc regulates macrophage migration.

A novel role for cystathionine gamma lyase in the control of p53: impact on endothelial senescence and metabolic reprograming

This paper identifies CSE-p53 interaction as a regulator of endothelial cell senescence and metabolic reprogramming in aging, showing that restoring this interaction can prevent senescence and promote vascular repair.

Msp1/ATAD1 restores mitochondrial function in Zellweger Spectrum Disease

The paper investigates peroxisomal dysfunction in Zellweger Spectrum Disease and shows that overexpressing ATAD1 restores mitochondrial function in patient-derived fibroblasts.

Loss of mitochondrial protease CLPP activates type I interferon responses through the mtDNA-cGAS-STING signaling axis

This study shows that CLPP deficiency causes mtDNA stress, which activates the cGAS-STING pathway and leads to type I interferon responses and antiviral gene expression.