Abstract
Autophagy is a lysosomal pathway that degrades and recycles unused or dysfunctional cell components as well as toxic cytosolic materials. Basal autophagy favors cell survival. However, the aberrant regulation of autophagy can promote pathological conditions. The autophagy pathway is regulated by several cell-stress and cell-survival signaling pathways that can be targeted for the purpose of disease control. In experimental models of disease, the carotenoid astaxanthin has been shown to modulate autophagy by regulating signaling pathways, including the AMP-activated protein kinase (AMPK), cellular homolog of murine thymoma virus akt8 oncogene (Akt), and mitogen-activated protein kinase (MAPK), such as c-Jun N-terminal kinase (JNK) and p38. Astaxanthin is a promising therapeutic agent for the treatment of a wide variety of diseases by regulating autophagy.
Highlights
Autophagy is a lysosomal pathway that degrades and recycles unused or dysfunctional cell components as well as toxic cytosolic materials
mitogen-activated protein kinase (MAPK), p38, extracellular-signal-regulated kinase (ERK), and Jun N-terminal kinase (JNK), and normalized the levels of their downstream effectors, such as Bax and Bcl-2. These results suggest that astaxanthin reduces autophagy by modulating MAPK-mediated Bax and Bcl-2 activation and the subsequent release of Beclin 1 [135]
Basal autophagy promotes cell survival, but aberrant autophagy, which occurs under pathological conditions, is deleterious
Summary
Autophagy, which literally means ‘to eat oneself’, is a catabolic process that degrades and recycles various cellular constituents, including dysfunctional organelles. The mammalian homolog of yeast Atg (mAtg9) is the major transport protein, which alternates between the PAS and peripheral donor sites, such as the trans-Golgi network and the endosomes [8]. Upon the induction of autophagy, mAtg transiently co-localizes with the PAS and transports membrane lipids from donor organelles to the phagophore, before returning to the peripheral sites around the trans-Golgi network where mAtg normally localizes [8,9]. Another transmembrane carrier protein, the vacuole membrane protein 1 (VMP1), induces the formation of ultrastructural features of autophagy and auophagosome formation [10]. Increased levels of autophagy constitute a protective response to certain diseased states as well to other sources of stress, such as nutrient starvation, oxidative stress, radiation, and hypoxia [28,29]
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