Inflamm-aging is a challenging and promising new branch of aging-related research fields that includes areas such as immunosenescence. Increasing evidence indicates that inflamm-aging is intensively associated with many aging diseases, such as Alzheimer's disease, atherosclerosis, heart disease, type II diabetes, and cancer. Mounting studies have focused on the role of inflamm-aging in disease progression and many advances have been made in the last decade. However, the underlying mechanisms by which inflamm-aging affects pathological changes and disease development are still unclear. Here, we review studies of inflamm-aging that explore the concept, pathological features, mechanisms, intervention, and the therapeutic strategies of inflamm-aging in disease progression.
Age is an independent risk factor of cardiovascular disease, even in the absence of other traditional factors.
Emerging evidence in experimental animal and human models has emphasized a central role for two main mechanisms
of age-related cardiovascular disease: oxidative stress and inflammation.
Excess reactive oxygen species (ROS) and superoxide generated by oxidative stress
and low-grade inflammation accompanying aging recapitulate age-related cardiovascular dysfunction,
that is, left ventricular hypertrophy, fibrosis, and diastolic dysfunction in the heart as well as endothelial dysfunction,
reduced vascular elasticity, and increased vascular stiffness. We describe the signaling involved in these two
main mechanisms that include the factors NF-κB, JunD, p66Shc, and Nrf2.
Potential therapeutic strategies to improve the cardiovascular function with aging are discussed, with a focus on calorie restriction, SIRT1, and resveratrol.
Accumulating evidence indicates that abnormal deposition of amyloid-b (Ab) peptide in the brain is responsible for endothelial cell damage and consequently leads to bloodbrain barrier (BBB) leakage. However, the mechanisms underlying BBB disruption are not well described. We employed an monolayer BBB model comprising bEnd.3 cell and found that BBB leakage was induced by treatment with Ab 1-42, and the levels of tight junction (TJ) scaffold proteins (ZO-1, Claudin-5, and Occludin) were decreased. Through comparisons of the effects of the different components of Ab 1-42 , including monomer (Ab 1-42 -Mono), oligomer (Ab 1-42 -Oligo), and fibril (Ab 1-42 -Fibril), our data confirmed that Ab 1-42 -Oligo is likely to be the most important damage factor that results in TJ damage and BBB leakage in Alzheimer's disease. We found that the incubation of bEnd.3 cells with Ab 1-42 significantly up-regulated the level of receptor for advanced glycation end-products (RAGE). Co-incubation of a polyclonal antibody to RAGE and Ab 1-42 -Oligo in bEnd.3 cells blocked RAGE suppression of Ab 1-42 -Oligo-induced alterations in TJ scaffold proteins and reversed Ab 1-42 -Oligoinduced up-regulation of RAGE, matrix metalloproteinase (MMP)-2, and MMP-9. Furthermore, we found that these effects induced by Ab 1-42 -Oligo treatment were effectively suppressed by knockdown of RAGE using small interfering RNA (siRNA) transfection. We also found that GM 6001, a broad-spectrum MMP inhibitor, partially reversed the Ab 1-42 -Oligo-induced inhibitor effects in bEnd.3 cells. Thus, these
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