What is Known of the Contribution of Cellular Senescence to Osteoporosis

The vast majority of senescent cells are produced when somatic cells reach the Hayflick limit to cell division, their telomeres shortened to a point at which they either self-destruct or enter the senescent state. Damage due to mutation or cytotoxic compounds can also induce senescence, as can the regenerative processes following injury. Senescent cells cease replication, become larger, and change their behavior in many other ways. Senescent cells secrete a pro-growth, pro-inflammatory mix of signals, the senescence-associated secretory phenotype (SASP), that attracts the attention of immune cells capable of destroying senescent cells, but also encourages nearby cells to become senescent. Throughout much of life, senescence serves as a way to remove damaged cells and suppress the risk of cancer, but this is only the case because these cells are promptly cleared as they arise. Unfortunately, the immune system becomes ever less capable with advancing age, and senescent cells accumulate as the pace of create outstrips the pace of destruction. When senescent cells are constantly present, the SASP turns from helpful to harmful. It induces chronic inflammation, disrupts tissue structure and function, and contributes meaningfully to the onset and progression of all of the common age-related conditions. One of those conditions is osteoporosis, the age-related loss of bone density and the subject of today's open access paper. Recent advances in senescence-associated secr...
Source: Fight Aging! - Category: Research Authors: Tags: Medicine, Biotech, Research Source Type: blogs