The impact of senescence on human health is a subject of profound significance in the realm of medical and biological sciences. Senescence, the natural process of aging, affects virtually every aspect of human health, from the cellular level to overall well-being. This intricate interplay between senescence and human health presents a multifaceted narrative that warrants exploration.

In adults, persistent senescence occurs due to three different scenarios on the basis of health condition. These are:
•      Senescence in normal aging
•      Disease related senescence
•      Therapeutic interventions
 
During normal and healthy aging, all individuals face tissue dysfunction. While age related disorders that are specific occurs to some people only. Senescent cells persist for longer times, making tissues less likely to perform adequately. These tissues become more susceptible and deteriorate faster in case of stressful conditions.
 
Due to lingering of senescent cells, the chances of disease onset might increase in case of stresses. For instance, cigarette smoke has constituents that can cause damage to DNA. This can trigger senescence. Disease related senescence is more or less restricted (constrained to some organs only) which is unlikely to normal senescence. The rate at which senescent cells accumulate in disease induced senescence is much higher as compared to normal aging. Similarly senescence can be as a consequence of treatment procedures such as irradiation and chemotherapy in treatment of cancer (tumour suppression). 
 
1. Senescence in normal aging
 
Senescence in normal cells can be detected based on some markers. However, most of the times it is difficult to locate senescent cells in tissues owing to the rare nature of these cells. The potentially non-specific markers include
•      Determination of cells having increased β-GAL activity
•      Overexpression of tumour suppressors such as p16Ink4a
 
Studies carried out in mice have shown that senescence is cells specific i.e. some cells have higher tendency of senescence than others. Aging correlates with senescence is explained by different experiments. This involves removal of genes associated with senescence programme i.e. CDKN2A and the activity of p16^Ink4a was suppressed by insertion of transgenes that have senescence suicidal activity. Due to this the aging activity in experimental animals (mice) was suppressed. 

Although this was a factor effecting aging process, but aging is considered more complicated than that. It is now thought that aging is more complex phenomenon. It involves certain nonphysiological characters that are expressed from early stages of development. Some factors that are involved with senescence as well as aging are DNA damage by telomere attrition, DNA damage by oxidative stress, ER stresses and other slowly occurring and accumulating damages involving certain macromolecules of body.
 
Further it was also noted that certain animals showing normal aging have abundance of senescent cells. The fact that either senescence is involved in natural aging or not is yet to be investigated further. Although there is not much evidence displaying a causal connection in natural aging and senescence, yet speculations can be made owing to the associations between cells in normal aging with senescent cells. In vitro studies suggests that there are two main dysfunctions of cells associated with senescence. These are as follows
•      The processes that are mainly involved in maintenance of tissues are disrupted because of SASP.
•      Reparative cells (such as stem and progenitor cells) are removed from proliferative pool as a consequence of senescence.
 
There are some other factors that supports that senescence is involved with process of aging. This includes presence of senescence-associated secretory phenotype factors in aging tissues such as some cytokines including TNFα and IL-6.
 
2. Senescence associated with age related diseases
 
There are a lot of researches that reported presence of senescent cells at sites of diseased organs but it is unknown that whether they trigger disease or are present as a consequence of disease. In various cases, diseases are caused due to loss of proliferation competent cells (such as in diabetic pancreas, glaucoma and osteoarthritis. While in other cases, disease related senescence is because of inflammation from senescence-associated secretory phenotype (SASP) such as in cancer and atherosclerosis. 
 
There is an interrelationship between senescence induced by chronic stresses and disease states. In young adulthood, some overwhelming exogenous external stressors cause diseases while maintaining normal functionality of tissues. For instance, if there are repetitive joint injuries in young adults, then the cartilage tissues lose their ability to repair causing osteoarthritis (as damage has surpassed the repair ability). In such cases, senescence is caused due to wear and tear caused by successive injuries. Moreover, whether these diseases occur at young age or at an elderly age, senescent cells are present in tissues.
 
 
3. Therapy induced senescence
 
Senescence is frequently considered as a therapeutic goal as it can be induced inform of stresses, such as use of ionizing radiations or chemotherapeutic treatment by causing DNA damage. Senescence can be used as a therapeutic treatment for cancer.
 
In cancer treatment, infrared radiations are given which shifts cells into state of senescence. This therapy induced senescence is characterized by various features such as growth arrest in cells for longer periods but these cells remain alive with normal metabolic activity. Apparently, these are more flattened and enlarged than normal cells. Also most of these cells attain polyploidy along with expression of marker b-galactosidase (senescent associated).
 
New researches are focusing on generating targeted therapies that induce senescence and cause apoptosis of cells. Such a therapy is made for promyelocytic leukemia in which oncogenic protein is blocked and p53 signalling is activated. This therapy is known as arsenic trioxide– retinoic acid therapy.