Aging involves changes at the level of intercellular communication and cell-autonomous alterations.

The intercellular communication occurs through direct interaction between cells and through both signals in an organism.

The single cells are dependent on the signals coming from other cells which, in their absence, are not able to survive.

In intercellular communication "inflammaging" results as the accumulation of inflammatory tissue damage.

The causes of the inflammation are:

the accumulation of pro-inflammatory tissue(1) damage,

dysfunctional immune system(2),

dysfunctional host cells(3).

Their consequences are: Obesity, type 2 Diabetes and Atherosclerosis.

A novel link between inflammation and aging derives from the recent finding that inflammatory and stress responses induce a reduction in the production of gonadotropin-releasing hormone (GnRH).
This GnRH decline can contribute to numerous aging-related changes such as bone fragility, muscle weakness, skin atrophy, and reduced neurogenesis.

At phenotypic level there are different alterations, which are caused from the failure of the immune system to clear infectious agents and from all the infected cells.

The immune system reacts with the recognition and the elimination of senescent cells.

In general the manipulations of one tissue could delay the aging of others; in fact these processes are progressive and coordinated with other tissues.

The other causes, of the defective intercellular communication, are at endocrine, neuroendocrine and neuronal level.

1- an intermediate cellular organizational level between cells and a complete organ.

2- a system of different biological structures, whose defense mechanisms have evolved to recognize and neutralize pathogens.

3- a living cell in which a virus reproduces.