Long Non-Coding RNAs and Macrophage Senescence in Age-Related Disease

Here, researchers review cellular senescence in macrophage cells and the biochemistry of long non-coding RNAs in macrophage senescence, a topic of great relevance to a number of age-related conditions, such as atherosclerosis. Cellular senescence takes place in most cell populations, in response to reaching the Hayflick limit on replication or in response to stress and damage. Senescent cells have important short-term roles to play, and near all destroy themselves or are destroyed by immune cells soon after entering the senescent state. These cells become harmful when they linger over long term, however, even in comparatively small numbers. They secrete a mix of signals, the senescence-associated secretory phenotype, that encourages other cells to become senescent, rouses the immune system to chronic inflammation, destructively remodels surrounding tissues, and more. The accumulation of senescent cells is one of the driving causes of degenerative aging. Cellular senescence is a particularly stable state of permanent cell cycle arrest. Macrophages, although terminally differentiated cells, do not undergo this type of replicative senescence and may hence undergo stress-induced senescence. In healthy conditions, macrophages maintain homeostasis; however, in pathological states, different stresses including DNA damage, telomere shortening, oncogene activation, impairment of some key proteins, and infections activate the p53, AIM2, and NF-κB signal pathways, initiating m...
Source: Fight Aging! - Category: Research Authors: Tags: Daily News Source Type: blogs