Cellular and systemic defense system against age-promoting stimuli.
نویسندگان
چکیده
Although much progress has been achieved in aging research using lower animals, especially yeast and C. elegans, aging in humans remains puzzling. Here I offer my hypothesis of host defense against age-promoting stimuli, which holds that the cell itself has a defense system and multi-organism, an even more sophisticated one against age-promoting stimuli. Here I review recent achievements in aging research and try to explain their findings in the light of my hypothesis. Age-promoting stimuli, including reactive oxygen species, telomere shortening or external stimuli such as UV or radiation induce stress responses in cells. The cellular defense system operates to overcome stimuli or repair damaged cellular components. Stress-induced damaged cells or infectious stimuli activate systemic defense systems, especially the innate immune system. Macrophages in the innate immune system are especially active not only in clearing damaged cells and repairing damaged tissue, but unfortunately, also in inducing age-related diseases.
منابع مشابه
Hepcidin and Host Defense against Infectious Diseases
Hepcidin is the master regulator of iron homeostasis in vertebrates. The synthesis of hepcidin is induced by systemic iron levels and by inflammatory stimuli. While the role of hepcidin in iron regulation is well established, its contribution to host defense is emerging as complex and multifaceted. In this review, we summarize the literature on the role of hepcidin as a mediator of antimicrobia...
متن کامل[The age-related macular degeneration as a vascular disease/part of systemic vasculopathy: contributions to its pathogenesis].
The wall of blood vessels including those in choroids may be harmed by several repeated and/or prolonged mechanical, physical, chemical, microbiological, immunologic, and genetic impacts (risk factors), which may trigger a protracted response, the so-called host defense response. As a consequence, pathological changes resulting in vascular injury (e. g. atherosclerosis, age-related macular dege...
متن کاملInduction of systemic resistance by plant growth promoting rhizobacteria in crop plants against pests and diseases
Plant growth promoting rhizobacteria (PGPR) belonging to Pseudomonas spp. are being exploited commercially for plant protection to induce systemic resistance against various pests and diseases. Mixtures of di!erent PGPR strains have resulted in increased e$cacy by inducing systemic resistance against several pathogens attacking the same crop. Seed-treatment with PGPR causes cell wall structural...
متن کاملInduction of Systemic Resistance against Aphids by Endophytic Bacillus velezensis YC7010 via Expressing PHYTOALEXIN DEFICIENT4 in Arabidopsis
Aphids are the most destructive insect pests. They suck the sap and transmit plant viruses, causing widespread yield loss of many crops. A multifunctional endophytic bacterial strain Bacillus velezensis YC7010 has been found to induce systemic resistance against bacterial and fungal pathogens of rice. However, its activity against insects attack and underlying cellular and molecular defense mec...
متن کاملA cry for help from leaf to root: above ground insect feeding leads to the recruitment of rhizosphere microbes for plant self-protection against subsequent diverse attacks.
Plants have evolved general and specific defense mechanisms to protect themselves from diverse enemies, including herbivores and pathogens. To maintain fitness in the presence of enemies, plant defense mechanisms are aimed at inducing systemic resistance: in response to the attack of pathogens or herbivores, plants initiate extensive changes in gene expression to activate "systemic acquired res...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Nagoya journal of medical science
دوره 68 1-2 شماره
صفحات -
تاریخ انتشار 2006