

Recent advances in genome sequencing and microarray technology have revealed that the human genome encodes thousands of long non-coding RNAs (lncRNAs). Very long RNA antisense to dimethylarginine dimethylaminohydrolase 1.senescence-associated secretory phenotype.metastasis-associated lung adenocarcinoma transcript 1.heterogeneous nuclear ribonucleoparticle.focally amplified lncRNA on chromosome 1.antisense non-coding mitochondrial RNA 2.Here we review our current knowledge of the mechanistic roles of lncRNAs affecting the main senescence pathways, and discuss the importance of identifying new regulators. 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. Many molecules have been identified as regulators of these two networks, such as transcription factors, chromatin modifiers and non-coding RNAs. Senescence is considered a tightly regulated stress response that is largely governed by the p53/p21 and p16/Rb pathways. Senescent cells are metabolically highly active, producing a wealth of cytokines and chemokines that, depending on the context, may have a beneficial or deleterious effect on the organism. Senescence may be induced by various stimuli such as telomere shortening, DNA damage or oncogenic insult, among others. Cellular senescence is a complex stress response that leads to an irreversible state of cell growth arrest.
