Abstract
Anemia and systemic signs of inflammation are common in elderly individuals and are associated with decreased survival. The common biological context for these two states is then the hallmarks of aging, i.e., genomic instability, telomere shortening, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication. Such aging-associated alterations of hematopoietic stem cells are probably caused by complex mechanisms and depend on both the aging of hematopoietic (stem) cells and on the supporting stromal cells. The function of inflammatory or immunocompetent cells is also altered by aging. The intracellular signaling initiated by soluble proinflammatory mediators (e.g., IL1, IL6 and TNFα) is altered during aging and contributes to the development of both the inhibition of erythropoiesis with anemia as well as to the development of the acute-phase reaction as a systemic sign of inflammation with increased CRP levels. Both anemia and increased CRP levels are associated with decreased overall survival and increased cardiovascular mortality. The handling of elderly patients with inflammation and/or anemia should in our opinion be individualized; all of them should have a limited evaluation with regard to the cause of the abnormalities, but the extent of additional and especially invasive diagnostic evaluation should be based on an overall clinical evaluation and the possible therapeutic consequences.
Highlights
The ageing global population is regarded as the most important present and future medical and social demographic problem worldwide by the World Health Organization [1]
The C-reactive protein (CRP) levels of this donor subgroup were further increased by stem cell mobilization by G-CSF, and our studies suggest that IL6 and possibly other members of the IL6 family can influence this systemic low-grade inflammation associated with aging
Aging is associated with the intrinsic and extrinsic modulation of hematopoiesis caused by age-associated alterations of hematopoiesis-supporting bone marrow stromal cells
Summary
The ageing global population is regarded as the most important present and future medical and social demographic problem worldwide by the World Health Organization [1]. The complex process of aging is characterized by the modulation of fundamental cellular processes, and this is reflected in the previously described nine hallmarks of aging, which include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion and altered intercellular communication (Figure 1) [2,3,4,5,6,7,8,9,10,11] These cellular effects lead to aging-dependent alterations in organs and tissues, including hematopoietic cells together with their supporting stromal cells in the common bone marrow microenvironment, as well as various immunocompetent cell subsets with the modulation of their immunoregulatory interactions [2,12,13,14,15,16]. We would expect the frequency and causes of anemia to differ between developed and underdeveloped countries; we emphasize that the present review is mainly based on studies in developed countries
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