In progeria syndromes and degenerative diseases, nuclear abnormalities are common. Preventing premature ageing and maintaining cell homeostasis both depend on selective autophagy of organelles. Although the nucleus serves as the cell's command centre by protecting our genetic information and regulating gene expression, little is known about nuclear autophagy. Here, we discuss new advancements in nuclear recycling, including nucleophagy in yeast physiology and mammalian pathological nucleophagic processes. The selective aspect of the degradation of nucleoli, DNA, and RNA in the nuclear envelope is highlighted.

The potential impact of disturbed nucleophagy on ageing and longevity is investigated. Also covered are the unresolved issues surrounding the circumstances, receptors, and substrates of homeostatic nucleophagy. Although it was once believed to be a bulk breakdown pathway, autophagy is actually a very selective cellular clearance mechanism. Macro-autophagy, micro-autophagy, and chaperone-mediated autophagy are the three main kinds of autophagy. In macro-autophagy, also known as autophagy, a double-membrane vesicle called the auto-phagosome is generated, which houses the substrates that will be broken down by hydrolytic enzymes in the lytic organelle, the lysosome.

Pexophagy, which is the selective degradation of peroxisomes, is an example of micro-autophagy. In this process, a portion of the organelle to be degraded pinches off and interacts directly with the lytic organelle or the lysosome. The material to be destroyed is guided to a receptor at the lysosome membrane by cytosolic chaperones in chaperone-mediated autophagy. Under physiological conditions, it occurs at low levels, but it can also be triggered by a variety of cellular stressors, including food restriction, oxidative stress, and DNA damage. The class III phosphatidylinositol-3-kinase complex, Vps15, Vps34, and Beclin-1 as well as the Unc-51-light kinase-1 (ULK1) complex assist in the formation of the phagophore during the initial phase of autophagy.

The production and maturation of auto-phagosomes, which are ultimately transported to and destroyed in the lysosome, is then dependent upon two ubiquitin conjugation systems, the microtubule-associated protein 1 light chain 3 (LC3) and autophagy related (Atg) Atg5-Atg7-Atg12 proteins. Additional autophagy receptors, such as p62 and NDP52, which have an LC3 interaction region recognised by LC3B confined to the outer auto-phagosomal membrane, are necessary for selective autophagy. Mitochondria and defective proteins are usually recycled in this manner. Under physiological conditions, it occurs at low levels, but it can also be triggered by a variety of cellular stressors, including food restriction, oxidative stress, and DNA damage.

The class III phosphatidylinositol-3-kinase complex, Vps15, Vps34, and Beclin 1 as well as the Unc-51-light kinase 1 (ULK1) complex assist in the formation of the phagophore during the initial phase of autophagy. The production and maturation of auto-phagosomes, which are ultimately transported to and destroyed in the lysosome, is then dependent upon two ubiquitin conjugation systems, the microtubule-associated protein 1 light chain 3 (LC3) and autophagy related (Atg) Atg5-Atg7-Atg12 proteins. Additional autophagy receptors, such as p62 and NDP52, which have an LC3 interaction region recognised by LC3B confined to the outer auto-phagosomal membrane, are necessary for selective autophagy.

Insights in Nutrition and metabolism is peer-reviewed that focuses on the topics include obesity, diabetes, metabolic syndrome, macro and micronutrients including vitamins and minerals, proteins and fats in addition to different food sources, recommended intake levels, nutritional deficiencies, toxicity, molecular and cellular biology of nutrients.

Authors can submit their manuscripts as an email attachment to nutrition@imedpubjournals.com

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