Thanks teaser great papers. I skimmed and found this interesting tidbit in the mito one.

Taken together, our data demonstrate that T3 maintains increased hepatic metabolic activity by promoting turnover of the intracellular pool of mitochondria through increased rates of mitophagy and mitochondrial synthesis. Thus, induction of mitophagy by intracellular ROS derived from increased mitochondrial energy production can help prevent the accumulation of damaged mitochondria as well as promote cellular health and function in hypermetabolic states. Mitochondrial function and its quality control are important factors in metabolic diseases such as diabetes and nonalcoholic fatty liver disease as well as aging.51,52 Our studies thus suggest that T3 or its analogs may be beneficial for treating these conditions by promoting mitochondrial turnover.53 Lastly, our finding that T3 stimulation of mitophagy occurs via a pathway involving increased ROS production; intracellular Ca2+ increase; CAMKK2, PRKAA1/AMPK, and ULK1 activation now provides several new therapeutic targets for maintaining mitochondrial number and function that could lead to novel treatments for metabolic and aging-related diseases.54