Why should autophagic flux be assessed?

Abstract

As autophagy is involved in cell growth, survival, development and death, impaired autophagic flux has been linked to a variety of human pathophysiological processes, including neurodegeneration, cancer, myopathy, cardiovascular and immune-mediated disorders. There is a growing need to identify and quantify the status of autophagic flux in different pathological conditions. Given that autophagy is a highly dynamic and complex process that is regulated at multiple steps, it is often assessed accurately. This perspective review article will focus on the autophagic flux defects in different human disorders and update the current methods of monitoring autophagic flux. This knowledge is essential for developing autophagy-related therapeutics for treating the diseases.

Essential role of autophagy in fucoxanthin-induced cytotoxicity to human epithelial cervical cancer HeLa cells

“…To assess autophagic flux, Baf A1, which is a potent and specific inhibitor of vacuolar H + -ATPases, was used to suppress the acidification of the lysosome and the autophagosome/ lysosome [15] . As shown in Figure 3A, Baf A1 significantly enhanced fucoxanthin-mediated GFP-LC3 patches.…”

Restoration of autophagic flux in myocardial tissues is required for cardioprotection of sevoflurane postconditioning in rats

“…Housekeeping levels of autophagy are required for normal cardiac action; however, the autophagy response to stimuli is either an adaptive response or a detrimental effect [9] . Autophagy is a dynamic process, beginning with the induction of autophagosome formation and ending with autophagosome degradation in lysosomes [17,18] . Autophagic flux is the pathway from the formation of autophagosomes to autolysosome degradation, which is determined by measuring the number of autophagosomes or autophagic markers over time in the presence and absence of autophagosome-lysosome fusion and lysosomal degradation inhibitors [19] .…”

The relevance of Nrf2 pathway and autophagy in pancreatic cancer cells upon stimulation of reactive oxygen species

“…For example, the increased autophagosomes could suggest either autophagic activation or an inhibition of lysosomal degradation [34]. Therefore, to further confirm that the silencing of Nrf2 promotes the progression of complete process of autophagy (autophagic flux) upon ROS stimulation in PANC-1 cells, we observed live cells infected with the Ad-mRFP-GFP-LC3 to differentiate the autophagosome and autolysosome during autophagy.…”