Engineered repeated electromagnetic field shock therapy for cellular senescence and age-related diseases.
A new consensus of gerontologists proposes that delay of biological senescence is the most potent public health measure for preventing chronic disease in late life. At the most fundamental level, cellular aging is characterized by a decline in repair and homeostatic systems. Thus, interventions that protect or rejuvenate these cellular systems hold significant promise for preventing or delaying the onset of age-related diseases. The most likely candidates for delaying senescence are the longevity-linked transcription factors DAF16 and HSF1. If one were to engineer negligible senescence, a key target would be the heat shock protein axis regulated by HSF1. This pathway is the preferred pathway to prevent protein damage or aggregation, whereas DAF-16/FOXO is a backup pathway activated during stress. Reduced HSF1 activity appears to accelerate tissue aging and shortens life span. Conversely, over-expression of HSF1 increases life span and decreases amyloid toxicity in animal models. This paper describes enhancement of the HSR/HSF1 pathway engineered by repeated electromagnetic field shock (REMFS). In a recent study, we demonstrated that REMFS therapy upregulates the HSR/HSF1 pathway, delays cellular senescence in young cells, and transiently reverses it in senescent cells, thus altering cellular mortality. The technology of applying certain beneficial EMF energy to the human body to stimulate the natural stress response and activate the repair and maintenance systems is a new strategy for engineered negligible senescence. We discuss the exciting clinical implications of REMFS therapy in human aging and disease.
Perez
Felipe P
FP
Department of Medicine, University of Illinois, College of Medicine, Chicago, IL 60612, USA. fperez04@uic.edu
Zhou
Ximing
X
Morisaki
Jorge
J
Ilie
John
J
James
Todd
T
Jurivich
Donald A
DA
D000375:Aging / Q000502:physiology; D016922:Cellular Senescence / Q000502:physiology*; D004268:DNA-Binding Proteins / Q000378:metabolism; D004574:Electromagnetic Fields; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D055909:Magnetic Field Therapy; D015398:Signal Transduction; D014157:Transcription Factors / Q000378:metabolism
D004268:DNA-Binding Proteins; C000619706:HSF1 protein, human; D000076249:Heat Shock Transcription Factors; D006360:Heat-Shock Proteins; D014157:Transcription Factors