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Stress‐induced rearrangements of cellular networks: Consequences for protection and drug design

2007/02/28 by Máté Szalay, Mate S. Szalay, I. Kovács +7 · 1 citation
Biochemistry, Genetics and Molecular Biology · #Bioinformatics and Genomic Networks #Gene Regulatory Network Analysis #Genetics, Aging, and Longevity in Model Organisms #q-bio.MN

paper · pdf · doi:10.1016/j.febslet.2007.03.083

published as FEBS Letters 581, 3675-3680 (2007) · 9 pages, 1 table, 2 figures, invited paper of FEBS Letters Cellular Stress special issue

openalex publication_date 2007/04/09 · arxiv created 2007/07/26 · arxiv updated 2009/12/01 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/28

Abstract

The complexity of the cells can be described and understood by a number of networks such as protein-protein interaction, cytoskeletal, organelle, signalling, gene transcription and metabolic networks. All these networks are highly dynamic producing continuous rearrangements in their links, hubs, network-skeleton and modules. Here we describe the adaptation of cellular networks after various forms of stress causing perturbations, congestions and network damage. Chronic stress decreases link-density, decouples or even quarantines modules, and induces an increased competition between network hubs and bridges. Extremely long or strong stress may induce a topological phase transition in the respective cellular networks, which switches the cell to a completely different mode of cellular function. We summarize our initial knowledge on network restoration after stress including the role of molecular chaperones in this process. Finally, we discuss the implications of stress-induced network rearrangements in diseases and ageing, and propose therapeutic approaches both to increase the robustness and help the repair of cellular networks.

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