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Autophagy mediates phase transitions from cell death to life. | LitMetric

Autophagy mediates phase transitions from cell death to life.

Heliyon

Department of Physics and Astronomy and Center for Theoretical Physics, Seoul National University, Seoul 151-747, South Korea.

Published: September 2015

AI Article Synopsis

  • Autophagy is a crucial process for cell maintenance, but its complexities in relation to human disease remain poorly understood.
  • Researchers aim to enhance understanding of autophagy by using computer analysis alongside traditional molecular studies.
  • The study proposes that autophagy influences cellular transitions that affect cell survival or death, linking molecular interactions to broader cellular behaviors.

Article Abstract

Autophagy is a lysosomal degradation pathway, which is critical for maintaining normal cellular functions. Despite considerable advances in defining the specific molecular mechanism governing the autophagy pathway during the last decades, we are still far from understanding the underlying principle of the autophagy machinery and its complex role in human disease. As an alternative attempt to reinvigorate the search for the principle of the autophagy pathway, we in this study make use of the computer-aided analysis, complementing current molecular-level studies of autophagy. Specifically, we propose a hypothesis that autophagy mediates cellular phase transitions and demonstrate that the autophagic phase transitions are essential to the maintenance of normal cellular functions and critical in the fate of a cell, i.e., cell death or survival. This study should provide valuable insight into how interactions of sub-cellular components such as genes and protein modules/complexes regulate autophagy and then impact on the dynamic behaviors of living cells as a whole, bridging the microscopic molecular-level studies and the macroscopic cellular-level and physiological approaches.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4939812PMC
http://dx.doi.org/10.1016/j.heliyon.2015.e00027DOI Listing

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