SENIOPROM asks AI to represent aging.
Aging is a complex process driving the progressive decline of functionality and regenerative potential of tissues. One hallmark of aging is cellular senescence, which leads to cellular dysfunction. Senescent cells accumulate and compromise tissue function by the secretion of pro-inflammatory molecules (also known as SASP). SASP components are known to drive pathogenesis and frailty.
Aging has puzzled scientists for a long time, now we have started to decipher it …
Recent evidence pinpoints mitochondrial and lysosomal dysfunction, disturbed inter-organelle communication, and a decline of proteostasis at various levels as key factors contributing to and shaping the senescence response; however, the underlying molecular and cellular mechanisms remain largely unknown. In addition, there is increasing understanding that the senescence phenotype is not uniform, a new concept intensely debated in recent literature.
The discovery that senescent cells drive aging in animal models has spurred huge research attempts to find pharmacological tools that may promote healthy aging by eliminating senescent cells or disabling their function in human tissues.
There is an increasing demand for the discovery of new classes of small molecules which would either avoid or postpone age-related disorders and disseases,
1) by selectively eliminating senescent cells from the body (i.e., “senolytics”) or;
2) inactivating damage-inducing properties of senescent cells, such as the SASP (i.e., “senomorphics”).
¿Where are we now?
The role of senescence in age-related dysfunction and disease, and its reversion to promote healthy aging.
With increasing age, senescent cells accumulate in several human tissues, due to a process known as cellular aging. Senescent cells secrete a cocktail of pro-inflammatory molecules known as the senescence-associated secretory phenotype (SASP). SASP components trigger changes in adjacent cells resulting in tissue remodeling and subsequently age-associated tissue dysfunction of human organs. Age-associated dysfunction in several tissues contributes to organismal aging.
Currently, small molecules with the potential to trigger the elimination of senescent cells (referred to as senolytics) or to dampen their detrimental influence on the organism (referred to as senostatics) are under development. Such compounds, with a potential for tissue rejuvenation, may provide new therapeutic opportunities for age-associated dysfunctions and diseases. Based on the beneficial effects of caloric restriction (CR) on human healthspan, compounds which mimic beneficial effects of caloric restriction may be particularly suitable candidates for the development of senolytics and/or senostatics.