The profound significance of autophagy as a cell survival mechanism under conditions of metabolic stress is a well-proven fact. Nearly a decade-long research in this area has led scientists to unearth various roles played by autophagy other than just being an auto cell death mechanism. It is implicated as a vital cell survival pathway for clearance of all the aberrant cellular materials in case of cellular injury, metastasis, disease states, cellular stress, neurodegeneration and so on. In this review, we emphasise the critical role of autophagy in the environmental stressors-induced neurotoxicity and its therapeutic implications for the same. We also attempt to shed some light on the possible protective role of autophagy in developmental neurotoxicity (DNT) which is a rapidly growing health issue of the human population at large and hence a point of rising concern amongst researchers. The intimate association between DNT and neurodegenerative disorders strongly indicates towards adopting autophagy activation as a much-needed remedy for DNT.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12035-016-9778-5DOI Listing

Publication Analysis

Top Keywords

autophagy activation
8
activation much-needed
8
much-needed remedy
8
cell survival
8
role autophagy
8
autophagy
5
adoptive autophagy
4
remedy chemical
4
chemical induced
4
induced neurotoxicity/developmental
4

Similar Publications

Background: Dysfunction in podocyte mitophagy has been identified as a contributing factor to the onset and progression of diabetic nephropathy (DN), and BMAL1 plays an important role in the regulation of mitophagy. Thus, this study intended to examine the impact of BMAL1 on podocyte mitophagy in DN and elucidate its underlying mechanisms.

Materials And Methods: High D-glucose (HG)-treated MPC5 cells was used as a podocyte injury model for investigating the potential roles of BMAL1 in DN.

View Article and Find Full Text PDF

Recent evidence links gut microbiota alterations to neurodegenerative disorders, including Parkinson's disease (PD). Replenishing the abnormal composition of gut microbiota through gut microbiota-based interventions "prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT)" has shown beneficial effects in PD. These interventions increase gut metabolites like short-chain fatty acids (SCFAs) and glucagon-like peptide-1 (GLP-1), which may protect dopaminergic neurons via the gut-brain axis.

View Article and Find Full Text PDF

Alpha-1 antitrypsin (AAT) deficiency (AATD) is a monogenic disease caused by misfolding of AAT variants resulting in gain-of-toxic aggregation in the liver and loss of monomer activity in the lung leading to chronic obstructive pulmonary disease (COPD). Using high-throughput screening, we discovered a bioactive natural product, phenethyl isothiocyanate (PEITC), highly enriched in cruciferous vegetables, including watercress and broccoli, which improves the level of monomer secretion and neutrophil elastase (NE) inhibitory activity of AAT-Z through the endoplasmic reticulum (ER) redox sensor protein disulfide isomerase (PDI) A4 (PDIA4). The intracellular polymer burden of AAT-Z can be managed by combination treatment of PEITC and an autophagy activator.

View Article and Find Full Text PDF

CK-666, an inhibitor of the actin-related protein complex 2/3 (Arp2/3), can suppress lamellipodia formation and cell migration. However, research on its application in tumor therapy is still limited. Using RNA-seq, we clustered and analyzed the functions of differentially expressed mRNAs in CK-666-treated tumor cells.

View Article and Find Full Text PDF

Background: Colorectal cancer (CRC) is one of the aggressive malignant tumors. Studies have shown that glycolysis promotes the proliferation of colorectal cancer cells and that PYCR2 is involved in cancer progression by affecting cellular glycolysis. In addition, PYCR2 is upregulated in colorectal cancer cell lines and can affect cellular autophagy.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!