Potential therapeutic applications of autophagy

By D. Rubinsztein, J. Gestwicki, Leon O. Murphy, D. Klionsky. Nature reviews. Drug discovery, 2007

1,053 citations recorded by the source corpus.

Subfields: Epidemiology, Pharmacology, Physiology

View Paper: https://www.semanticscholar.org/paper/9731efa4ba787e41eddc77ac0092658ab2488848

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Citations in the corpus

Inhibition of mTOR by Rapamycin Abolishes Cognitive Deficits and Reduces Amyloid-β Levels in a Mouse Model of Alzheimer's Disease (2010, background): “aggregated proteins[18] such as those that cause multiple neurodegenerative diseases including AD.”
Exosomal cell-to-cell transmission of alpha synuclein oligomers (2012, background): “Autophagy can function as a protective mechanism in cells and is particularly crucial in the aging brain and in neurodegeneration where aggregated proteins accumulate [100].”
Autophagy: cellular and molecular mechanisms (2010, background): “However, TOR can function as the catalytic component of two distinct complexes, known as TORC1 and TORC2, and rapamycin appears to have greater inhibitory activity against TORC1, driving the search for so-called ‘rapalogs’ that target both TORC1 and TORC2 [76].”
Discovery of drug mode of action and drug repositioning from transcriptional responses (2010, background): “We focused on identifying drugs that could enhance autophagy, a key biological process involved in cancer and in infectious and neurodegenerative diseases (38).”
Novel targets for Huntington’s disease in an mTOR-independent autophagy pathway (2008, background): “While the narrow pore of the proteasome barrel precludes clearance of large membrane proteins and protein complexes (including oligomers and aggregates), mammalian lysosomes can degrade protein complexes and organelles by macroautophagy, generally referred to as autophag”
TFEB-mediated autophagy rescues midbrain dopamine neurons from α-synuclein toxicity (2013, background): “The role of autophagy in the elimination of toxic protein species has generated interest in the development of therapeutic strategies for neurological diseases characterized by protein misfolding and aggregation (4, 24, 25).”
Small molecules enhance autophagy and reduce toxicity in Huntington's disease models. (2007, methodology): “Virgin female flies of genotype y w; gmr-httNterm(1-171)Q120 (gmrQ120)22 were mated with isogenised w1118 males28 in food vials for 48 h.”
Cannabinoid action induces autophagy-mediated cell death through stimulation of ER stress in human glioma cells. (2009, background): “In many cellular settings, triggering of autophagy relies on the inhibition of mammalian target of rapamycin complex 1 (mTORC1), an event that promotes the activation (de-inhibition) of several autophagy proteins (Atgs) involved in the initial phase of membrane isolation (1).”
Role of autophagy in cancer (2007, background): “This approach has shown promise in the treatment of degenerative disorders that are linked to aberrant protein accumulation, such as Huntington's disease, that is reliant on autophagy for the removal of aggregated mutant protein”
Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, background): “Autophagy is a highly regulated process that can either be involved in the turnover of long-lived proteins and whole organelles in a generalized fashion or can specifically target distinct organelles (for example, mitochondria in mitophagy and the endoplasmic reticulum (ER) in reticulophagy), thereb”
Pancreatic cancers require autophagy for tumor growth. (2011, positive): “As shown in Figure 1B, inhibiting autophagosome degradation by CQ, which blocks lysosomal acidification and autophagosome degradation (Rubinsztein et al. 2007), further increased the number of GFP-LC3 puncta in PDAC lines.”
Autophagy in the pathogenesis of disease. (2008, positive): “Lithium chloride, a drug used for the treatment of bipolar disorder, induces autophagy by reducing IP3 levels and enhances the clearance of aggregate-prone proteins (Rubinsztein et al., 2007).”