Hif1α-dependent mitochondrial acute O sensing and signaling to myocyte Ca channels mediate arterial hypoxic vasodilation.

Vasodilation in response to low oxygen (O) tension (hypoxic vasodilation) is an essential homeostatic response of systemic arteries that facilitates O supply to tissues according to demand. However, how blood vessels react to O deficiency is not well understood. A common belief is that arterial myocytes are O-sensitive.

Microglia mitochondrial complex I deficiency during development induces glial dysfunction and early lethality.

Primary mitochondrial diseases (PMDs) are associated with pediatric neurological disorders and are traditionally related to oxidative phosphorylation system (OXPHOS) defects in neurons. Interestingly, both PMD mouse models and patients with PMD show gliosis, and pharmacological depletion of microglia, the innate immune cells of the brain, ameliorates multiple symptoms in a mouse model. Given that microglia activation correlates with the expression of OXPHOS genes, we studied whether OXPHOS deficits in microglia may contribute to PMDs.

Carotid Body Function in Tyrosine Hydroxylase Conditional Olfr78 Knockout Mice.

The gene encodes a G-protein-coupled olfactory receptor that is expressed in several ectopic sites. is one of the most abundant mRNA species in carotid body (CB) glomus cells. These cells are the prototypical oxygen (O) sensitive arterial chemoreceptors, which, in response to lowered O tension (hypoxia), activate the respiratory centers to induce hyperventilation.

Mitochondrial integrated stress response controls lung epithelial cell fate.

Alveolar epithelial type 1 (AT1) cells are necessary to transfer oxygen and carbon dioxide between the blood and air. Alveolar epithelial type 2 (AT2) cells serve as a partially committed stem cell population, producing AT1 cells during postnatal alveolar development and repair after influenza A and SARS-CoV-2 pneumonia. Little is known about the metabolic regulation of the fate of lung epithelial cells.