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Cellular senescence is a complex stress response that leads to an irreversible state of cell growth arrest. Senescence may be induced by different stimuli such as telomere shortening, DNA damage or oncogenic insult among others. Senescent cells are metabolically highly active producing a wealth of cytokines and chemokines that depending on the context may have a beneficial or deleterious impact on the organism. Senescence is considered a tightly regulated stress response that is largely governed by the p53/p21 and p16/Rb pathways. Many molecules have been identified as regulators of these two networks, such as transcription factors, chromatin modifiers and recently, non-coding RNAs. The expression level of several long non-coding RNAs is affected during different types of senescence, however, which of these are important for the biological function remains poorly understood. We review here our current knowledge of the mechanistic roles of lncRNAs affecting the main senescence pathways and discuss the importance of identifying new regulators. This article is protected by copyright. All rights reserved.