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https://www.selleckchem.com/products/a-83-01.html Cellular senescence is mainly characterized as a stable proliferation arrest and a senescence associated secretory phenotype (SASP). Senescence is triggered by diverse stimuli such as telomere shortening, oxidative stress, oncogene activation and DNA damage, and consequently contributes to multiple physiology and pathology outcomes, including embryonic development, wound healing and tumor suppression as well as aging or age-associated diseases. Interestingly, therapeutic clearance of senescent cells in tissues has recently been demonstrated to be beneficial for extending a healthy lifespan and for improving numerous age-related disorders. However the molecular mechanisms of senescence regulation remain partially understood. Theoretically, senescence is tightly regulated by a vast number of molecules, among which the p16 and p53 pathways are the most classical. In addition, intracellular cellular calcium signaling has emerged as a key regulator of senescence. In the last few decades, a growing number of studies have demonstrated that microRNAs (miRNAs, small non-coding RNAs) are strongly implicated in controlling senescence, especially at the transcriptional and post-transcriptional levels. In this review we will discuss the involvement of miRNAs in modulating senescence through the major p16, p53, SASP and calcium signaling pathways, thus aiming to reveal the mechanisms of how miRNAs regulate cellular senescence.Hepcidin is a peptide hormone which helps in regulating iron homeostasis in the human body. Iron obtained from daily diet is passed through the intestinal enterocyte apical membrane via divalent metal transporter 1 (DMT1), which is either stored as ferritin or moved into the plasma by hepcidin-ferroportin (Fpn) as an exporter. Hepcidin (hepatic bactericidal protein) is a cysteine rich peptide, was initially identified as a urinary antimicrobial peptide. It contains 25 amino acids and four disulfide bridges. I

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