Nuclear abnormalities are prominent in degenerative disease and progeria syndromes. Selective autophagy of organelles is instrumental in maintaining cell homeostasis and prevention of premature ageing. Although the nucleus is the control centre of the cell by safeguarding our genetic material and controlling gene expression, little is known in relation to nuclear autophagy. Here we present recent discoveries in nuclear recycling, namely nucleophagy in physiology in yeast and nucleophagic events that occur in pathological conditions in mammals. The selective nature of degrading nuclear envelope components, DNA, RNA and nucleoli is highlighted. Potential effects of perturbed nucleophagy in senescence and longevity are examined. Moreover, the open questions that remain to be explored are discussed concerning the conditions, receptors and substrates in homeostatic nucleophagy.

Cell homeostasis requires the concerted action of cellular pathways involved in degradation, trafficking and intercellular communication, which are interlinked to satisfy the cell's needs upon demand. Defects in these pathways instigate the development of several age-related pathologies, such as neurodegenerative and chronic inflammatory diseases. Autophagy is an evolutionarily conserved and tightly regulated process of degrading cellular constituents. The endosomal and vesicular trafficking pathways contribute to this regulation and share common features with the autophagic process. Recently, autophagy has been implicated in the endosome/exosome secretory pathway. Importantly, current technological advances allow the manipulation of exosomes as drug nanocarriers in pharmaceutical intervention strategies. Here, we survey emerging findings relevant to the crosstalk between autophagy and the endo/exosomal vesicular trafficking pathways. In addition, we discuss novel methodologies that have recently been developed, which allow the utilization of these pathways for targeted drug delivery in disease.

Autophagy is a universal cellular homeostatic process, required for the clearance of dysfunctional macromolecules or organelles. This self-digestion mechanism modulates cell survival, either directly by targeting cell death players, or indirectly by maintaining cellular balance and bioenergetics. Nevertheless, under acute or accumulated stress, autophagy can also contribute to promote different modes of cell death, either through highly regulated signalling events, or in a more uncontrolled inflammatory manner. Conversely, apoptotic or necroptotic factors have also been implicated in the regulation of autophagy, while specific factors regulate both processes. Here, we survey both earlier and recent findings, highlighting the intricate interaction of autophagic and cell death pathways. We, Furthermore, discuss paradigms, where this cross-talk is disrupted, in the context of disease.