The accumulation of SIRT4 in the nuclei of kidney cells drives kidney fibrosis, so blocking the movement of this protein could be a potential therapeutic strategy against fibrosis.
Cell biology and animal model analysis in mice shows that molecules involved in glycolytic metabolism could potentially serve as therapeutic targets for the treatment of neurological diseases.
In a mouse model of Sjogren's disease, mitochondrial function and Ca2+ signaling are disrupted resulting in altered coupling between Ca2+ release and Ca2+ activated Cl- channels and salivary gland hypofunction.
PINK1 deficiency in Parkinson's disease models causes toxic oxidized and iron-depleted CISD1 yet CISD1 removal benefits PINK1 mutant Drosophila indicating its potential as a therapeutic target for mitochondrial dysfunction and neurodegeneration.
