Sabine Schulz

TL;DR: A mouse model recapitulating key features of human metabolic syndrome, NASH, and HCC by long-term feeding of a choline-deficient high-fat diet is developed, demonstrating that distinct molecular mechanisms determine NASH and H CC development.

TL;DR: It is suggested that the mitochondrion constitutes a pivotal target of copper in Wilson disease, and copper-chelating agents reversed mitochondrial accumulation of copper, as well as signs of intra-mitochondrial membrane crosslinking, thereby preserving the functional and structural integrity of mitochondria.

TL;DR: This is the first study showing the biological alterations in the murine heart mitochondria several weeks after the exposure to low- and high-dose of ionizing radiation, and it is proposed that these first pathological changes lead to an increased risk of cardiovascular disease after radiation exposure.

TL;DR: It is demonstrated that ATP7B-deficient rats recapitulate WD-associated phenotypes, including hepatic copper accumulation, liver damage, and mitochondrial impairment, and methanobactin treatment prevented hepatocyte death, subsequent liver failure, and death in the rodent model, suggesting that MB has potential as a therapeutic agent for the treatment of acute Wilson disease.

TL;DR: It is concluded that archazolid leads to energy stress which activates adaptive mechanisms like autophagy mediated by HIF1α and finally leads to apoptosis which is proposed as a promising drugable target in cancer therapy caught up at the interplay of apoptosis, Autophagy, and cellular/metabolic stress.