Aspartate metabolism in endothelial cells activates the mTORC1 pathway to initiate translation during angiogenesis.

Angiogenesis, the active formation of new blood vessels from pre-existing ones, is a complex and demanding biological process that plays an important role in physiological as well as pathological settings. Recent evidence supports cell metabolism as a critical regulator of angiogenesis. However, whether and how cell metabolism regulates endothelial growth factor receptor levels and nucleotide synthesis remains elusive.

Activation of the Nrf2 Pathway as a Therapeutic Strategy for ALS Treatment.

Amyotrophic lateral sclerosis is a progressive and fatal disease that causes motoneurons degeneration and functional impairment of voluntary muscles, with limited and poorly efficient therapies. Alterations in the Nrf2-ARE pathway are associated with ALS pathology and result in aberrant oxidative stress, making the stimulation of the Nrf2-mediated antioxidant response a promising therapeutic strategy in ALS to reduce oxidative stress. In this review, we first introduce the involvement of the Nrf2 pathway in the pathogenesis of ALS and the role played by astrocytes in modulating such a protective pathway.

UBIAD1 and CoQ10 protect melanoma cells from lipid peroxidation-mediated cell death.

Cutaneous melanoma is the deadliest type of skin cancer, although it accounts for a minority of all skin cancers. Oxidative stress is involved in all stages of melanomagenesis and cutaneous melanoma can sustain a much higher load of Reactive Oxygen Species (ROS) than normal tissues. Melanoma cells exploit specific antioxidant machinery to support redox homeostasis.

Adaptive redox homeostasis in cutaneous melanoma.

Cutaneous melanoma is the most aggressive type of skin cancer. Although cutaneous melanoma accounts for a minority of all types of skin cancer, it causes the greatest number of skin cancer related deaths worldwide. Oxidative stress and redox homeostasis have been shown to be involved at each stage of a malignant melanocyte transformation, called melanomagenesis, as well as during drug resistance.

Mitochondrial Deacetylase Sirt3 Reduces Vascular Dysfunction and Hypertension While Sirt3 Depletion in Essential Hypertension Is Linked to Vascular Inflammation and Oxidative Stress.

Rationale: Hypertension represents a major risk factor for stroke, myocardial infarction, and heart failure and affects 30% of the adult population. Mitochondrial dysfunction contributes to hypertension, but specific mechanisms are unclear. The mitochondrial deacetylase Sirt3 (Sirtuin 3) is critical in the regulation of metabolic and antioxidant functions which are associated with hypertension, and cardiovascular disease risk factors diminish Sirt3 level.