Eaten alive: a history of macroautophagy
By Zhifen Yang, D. Klionsky. Nature Cell Biology, 2010
2,122 citations recorded by the source corpus.
Macroautophagy (hereafter autophagy), or 'self-eating', is a conserved cellular pathway that controls protein and organelle degradation, and has essential roles in survival, development and homeostasis. Autophagy is also integral to human health and is involved in physiology, development, lifespan and a wide range of diseases, including cancer, neurodegeneration and microbial infection. Although research on this topic began in the late 1950s, substantial progress in the molecular study of autophagy has taken place during only the past 15 years. This review traces the key findings that led to our current molecular understanding of this complex process.
Subfields: Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/0145924010c0d2a8ac49aef1ee202226a4076a58
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
In Physiology
Citations in the corpus
- Pathological Ventricular Remodeling: Mechanisms: Part 1 of 2 (2013, background): “Cumulative organelle damage with age may also increase the need for clearance by autophagy, a process that declines with age.(51) Cardiomyocyte hypertrophy is more pronounced in aged heart, contributing to cardiac dysfunction,(167) and the intrinsic capacity of the heart to regenerate diminishes wit”
- Target of Rapamycin (TOR) in Nutrient Signaling and Growth Control (2011, background): “Autophagy is conserved across eukarya, and there is much interest in understanding how macroautophagy is regulated as it has been linked to several pathologies including cancer, neurological disorders, and longevity (Yang and Klionsky 2010).”
- Pathophysiology of Myocardial Infarction (2015, neutral): “The term “autophagy” describes the process by which dysfunctional or unnecessary components of the cell are delivered to lysosomes for degradation (402).”
- Emerging regulation and functions of autophagy (2013, background): “The identification of the Atg proteins in autophagy was a milestone in the understanding of the importance of this process 1, 9 .”
- An Overview of Autophagy: Morphology, Mechanism, and Regulation (2014, methodology): “This figure was modified from Figure 1 in Yang and Klionsky (153).”
- Human Coronavirus: Host-Pathogen Interaction. (2019, background): “Specifically, cells under stress conditions (such as starvation, growth factor deprivation, or infection by pathogens) initiate autophagy in nucleation sites at the ER,where part of the cytoplasm and/or organelles are sequestered in DMVs (autophagosomes) and degraded by fusing with lysosomes (135).”
- p62 links the autophagy pathway and the ubiqutin–proteasome system upon ubiquitinated protein degradation (2016, neutral): “It was first considered to be a non-selective bulk system for degrading long-lived proteins and organelles to recycle nutrients and generate energy [12].”
- Erratum: Autophagy suppresses tumorigenesis through elimination of p62 (Cell (2009) 137 (1062-1075)) (2011, neutral): “Autophagy, which is normally induced by starvation or stress, targets cellular proteins, protein aggregates and organelles for degradation in lysosomes[1].”
- MTORC1 functions as a transcriptional regulator of autophagy by preventing nuclear transport of TFEB (2012, background): “Under starvation conditions when MTORC1 is inactivated, MTORC1 dissociates from the ULK complex, thus leading to autophagy induction.(8) In addition, many cellular pathways known to regulate autophagy merge on MTORC1.”
- Autophagy modulation as a potential therapeutic target for diverse diseases (2012, neutral): “Lifestyle factors and colorectal cancer risk (2): a systematic review and meta‐analysis of associations with leisure‐time physical activity.”