Chronic Inflammation Potentiates Kidney Aging
Section snippets
The Association of Chronic Inflammation with Aging and Aging Renal Function Decline
Accumulating evidence suggests that aging often represents a state of chronic low-grade inflammation characterized by increased serum levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-1–receptor antagonist, fibrinogen, and C-reactive protein (CRP).6, 7, 8 For instance, the levels of fibrinogen and CRP were higher in healthy elders older than 60 years than in adults younger than 45 years.7 Chronic inflammation may play an important role in aging-related diseases such as
The Cellular Sources of Chronic Inflammation in Aging
The cellular basis of chronic inflammation in aging is unknown. A dysregulation of the immune system in aging is believed to play an important role in chronic inflammation.14 Generally, the functions of immune cells are decreased in older people. Fewer B and T cells are produced in older human beings.14, 15 In addition, B cells from older individuals generated antibodies with lower affinity to antigen and had an impaired ability to undergo class-switch recombination compared with B cells from
The Underlying Mechanisms of Chronic Inflammation in Aging
Oxidative stress is implicated as a critical factor for aging and aging-related chronic inflammation. The levels of reactive oxygen and nitrogen species are increased in aging in all the organs, including the kidney, owing to excessive production of free radicals and decreased anti-oxidant defenses. Free radicals or nonradical oxidants constantly are generated by aerobic metabolism and may be an element of some signaling events such as transducing proliferative signals from platelet-derived
A Role of Chronic Inflammation in Kidney Aging
Although 24% of individuals age 65 years and older have decreased renal function, very few develop end-stage renal disease unless there is a second injury, suggesting that kidney aging is either a slowly progressing process or that the current method of measuring renal function overestimates the degree of renal functional loss in aging. This slow progression is mirrored in aging C57B6 mice, a model of kidney aging.24 Because aging could be defined more clearly in females by cessation of ovarian
Conclusions and Future Directions
The advances made in recent years in ROS signaling, T-cell immunobiology, and cell senescence have clarified some of the molecular mechanisms and cellular aspects of chronic inflammation in aging. In addition, extensive studies on the mechanisms of calorie restriction in prolonging life span and preventing organ aging have led to the identification of nicotinamide adenine dinucleotide (NAD(+))-dependent histone deacetylases sirtuins as an important subgroup of molecules that actively are
Acknowledgment
The authors thank Dr. Gary Striker for critical reading of and comments on the manuscript.
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2019, International Journal of Biochemistry and Cell BiologyCitation Excerpt :Dental pulp inflammation could cause premature cellular senescence through oxidative stress and DNA damage responses (Feng et al., 2014; Dierick et al., 2002). On the other hand, the aging process often leads to chronic inflammation and senescent DPCs upregulated the expression of chronic inflammatory molecules (Mei, 2009; Cesari et al., 2004). In addition, a recent study showed that sclerostin deficiency could accelerate the formation of reparative dentin in a pulp injury model (Collignon et al., 2017).
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Supported by National Institutes of Health grant 5R01AG027628-03 (F.Z.).