Low-level inflammation can smolder in your body without any symptoms. This can indicate that you have underlying health problems that need attention.
Redefining Chronic Inflammation in Aging and Age-Related Diseases: Proposal of the Senoinflammation Concept
Below are some quotes from this study showing that researchers are focusing on systemic inflammation as a key driver of aging:
One interesting recent study has reported the activation of NF-κB occurs in the hypothalamus during aging . The authors of this paper suggested that chronic activation of NF-κB signaling causes hypothalamic inflammation, which then affects whole-body metabolism, in particular, the endocrine regulation of glucose and lipid metabolism .
These findings render support for the possibility that dysregulated local tissue inflammation affects the systemic metabolic responses of the whole organism. These new revelations indicate that increased cellular inflammatory signaling pathways and tissue inflammation can propagate to systemic inflammation during the aging process.
Chronic inflammation is causally associated with changes in the cellular redox state and cell death signaling pathways.
One of the major changes that occur during aging is the dysregulation of the immune response, leading to a chronic systemic inflammatory state.
Elevated levels of chemokines and C-reactive protein (CRP) have been found to be involved in age-related pathogenesis.
Several key intra- or inter-cellular signaling pathways are closely associated with age-related chronic inflammatory changes during aging.
Chronic inflammation is so widely and deeply involved in many age-related chronic disorders such as atherosclerosis, diabetes, obesity, sarcopenia, and Alzheimer’s disease.
Altered cellular signaling systems that underlie chronic inflammation during aging. These signaling pathways include the insulin and insulin-like growth factor (IGF) pathways, 5′-AMP-activated protein kinase (AMPK)-mechanistic target of rapamycin (mTOR) pathway, Forkhead box O (FOXO) families, sirtuin (SIRT), and p53-related pathways.
Increased systemic inflammation is closely associated with aging and age-related chronic diseases.
It is now well recognized that adipose tissue is one of the major sites involved in systemic inflammation.
Two to four-fold elevations in the circulating levels of inflammatory cytokines, such as TNF-α, IL-6, and IL-1β, CRP and serum amyloid A, are typically observed in the elderly or aged animal compared to the young.
These observations are noteworthy because the levels of cytokines increase even in healthy individuals in the absence of acute infection or diseases.
Age-associated increases in systemic inflammation are associated with, and predictive of, many aging phenotypes
Proinflammatory mediators can interact with one another and the magnitude of this interaction increases as the level of proinflammatory mediators increases. For example, TNF-α plays an important role in the production of IL-6 by activating several pathways, and IL-6 is a major factor in the elevation of CRP levels found in older adults.
Inflammation is an underlying cause of cardiac dysfunction.
Chronic inflammation is an underlying cause of age-related neurodegenerative diseases.
Chronic inflammation is involved in cancer, which has been of tremendous interest after the discovery that inflammation plays an important role in tumor progression.
Strongly suggests that NF-κB, the central core inflammatory mediator, is a key transcriptional factor in the initiation and progression of cancer.
Newly emerging data has revealed that age-related chronic inflammation is much more widely and heavily involved in many cellular activities than previously thought.
Decreased autophagic function is implicated in age-related inflammation.
It is important noting that these age-related changes in adiposity, autophagy, and inflammasome that exacerbate age-related chronic systemic inflammation are not considered in the current, conventional, view of chronic inflammation.
Inflammation underlies the onset and progression of metabolic syndrome.
ER stress and insulin resistance are associated with lipid accumulation, leading to an exacerbation of inflammation and age-associated chronic inflammation.