Inflamaging results from decreased antioxidant capacity and thereby decreases resilience.
Integral in this process is ROS that trigger the inflammatory cascade of the inflamasome, the innate immune system. NLRP3, caspase and il-beta 1 form heteromers of inflammation in conjunction with inflammatory molecules notably the c reactive protein.
Macrophages are the sentinels mentioned below. Microglia cells in brain. Muller cells in retina. Kuppfer cells in liver. M1 cells in endothelial linings of arteries and veins, respiratory linings, gastrointestinal linings, pancreatic and biliary duct linings.
The most effective upstream fix to molecular inflamaging is increased antioxidant capacity via Nrf2 activators and spermidine/wheat germ enhancement of proteostasis.
Nrf2 activators include melatonin, hydrogen rich water, sulforaphane, spermidine/wheat germ and Green tea extract.
As critical proof of this concept Reversing Dementia accomplished over a thousand times by Dale Bredesen MD of the Buck Institute SHOUTS special cause variation from usual practice. It signals a paradigm shift to make cells more resilient and resistant to molecular AND injury related INFLAMMATION!
See his YouTube talk and review his book. His results are not chance alone. They are reproducible and have relevance to every organ based specialist and organ based disease model of modern medicine.
It’s time to redefine inflammation
+ Author Affiliations
- ↵1Correspondence: Division of Rheumatology, Case Western Reserve University at MetroHealth Medical Center, 2500 MetroHealth Dr., Cleveland, Ohio, 44109 USA. E-mail: ixk2@case.edu
Abstract
Inflammation has been defined for many years as the response to tissue injury and infection. We are now forced to reconsider this definition by the avalanche of reports that molecules and cells associated with inflammation are activated or expressed in high concentration in a large variety of states in the absence of tissue injury or infection. Modest increases in concentration of C-reactive protein, a circulating marker of inflammation, have been reported to be associated with an astounding number of conditions and lifestyles felt to be associated with poor health; these conditions represent or reflect minor metabolic stresses. In recent years we have learned that inflammation is triggered by sentinel cells that monitor for tissue stress and malfunction—deviations from optimal homeostasis—and that molecules that participate in the inflammatory process play a role in restoring normal homeostasis. Accordingly, we suggest that inflammation be redefined as the innate immune response to potentially harmful stimuli such as pathogens, injury, and metabolic stress.—Antonelli, M., Kushner, I. It’s time to redefine inflammation.
- CREBH
- cyclic AMP response element-binding protein-H
- CRP
- C-reactive protein
- ER
- endoplasmic reticulum
- TLR
- Toll-like receptor
- UPR
- unfolded protein response
- Received December 12, 2016.
- Ac.
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