Stress eating: Autophagy targets nuclear pore complexes.

Lee et al. (2020. Nat.

Mechanisms of Autophagy in Metabolic Stress Response.

Autophagy is a highly conserved catabolic pathway critical for stress responses and the maintenance of cellular homeostasis. Defective autophagy contributes to the etiology of an increasing number of diseases including cancer, neurodegeneration, and diabetes. Cells have to integrate complex metabolic information in order to counteract metabolic challenges ranging from carbon, nitrogen, and phosphate to metal ion limitations.

Acetyl-CoA carboxylase 1-dependent lipogenesis promotes autophagy downstream of AMPK.

Autophagy, a membrane-dependent catabolic process, ensures survival of aging cells and depends on the cellular energetic status. Acetyl-CoA carboxylase 1 (Acc1) connects central energy metabolism to lipid biosynthesis and is rate-limiting for the synthesis of lipids. However, it is unclear how lipogenesis and its metabolic consequences affect autophagic activity.

Aspirin impairs acetyl-coenzyme A metabolism in redox-compromised yeast cells.

Aspirin is a widely used anti-inflammatory and antithrombotic drug also known in recent years for its promising chemopreventive antineoplastic properties, thought to be mediated in part by its ability to induce apoptotic cell death. However, the full range of mechanisms underlying aspirin's cancer-preventive properties is still elusive. In this study, we observed that aspirin impaired both the synthesis and transport of acetyl-coenzyme A (acetyl-CoA) into the mitochondria of manganese superoxide dismutase (MnSOD)-deficient Saccharomyces cerevisiae EG110 yeast cells, but not of the wild-type cells, grown aerobically in ethanol medium.

Dietary spermidine for lowering high blood pressure.

Loss of cardiac macroautophagy/autophagy impairs heart function, and evidence accumulates that an increased autophagic flux may protect against cardiovascular disease. We therefore tested the protective capacity of the natural autophagy inducer spermidine in animal models of aging and hypertension, which both represent major risk factors for the development of cardiovascular disease. Dietary spermidine elicits cardioprotective effects in aged mice through enhancing cardiac autophagy and mitophagy.

Cardioprotection and lifespan extension by the natural polyamine spermidine.

Aging is associated with an increased risk of cardiovascular disease and death. Here we show that oral supplementation of the natural polyamine spermidine extends the lifespan of mice and exerts cardioprotective effects, reducing cardiac hypertrophy and preserving diastolic function in old mice. Spermidine feeding enhanced cardiac autophagy, mitophagy and mitochondrial respiration, and it also improved the mechano-elastical properties of cardiomyocytes in vivo, coinciding with increased titin phosphorylation and suppressed subclinical inflammation.