Aging & Gerontology

Abstract

A large amount of evidence shows that aging is not the result of random damage that gradually accumulates. The “telomere DNA and ribosomal DNA co-regulation model for cell senescence” suggests that aging is a genetic program driven by telomeres and rDNA through the p53 pathway. The fundamental cause of cellular aging and the Hayflick limit lies in the co-regulation of telomeres and rDNA. Therefore, the best way to reverse aging and significantly extend lifespan is to increase the length of telomeres and rDNA arrays in adult stem cells within tissues.

Biography

· When I was 8 years old, I saw a clay pot containing a dead man's skull in a ravine not far from my home. The surface of the clay pot was covered with green moss, and I felt cold, and I realized that one day I would also be placed in a dark clay pot, forever and forever. What a horror! Then came the idea of conquering aging. After I graduated from primary school, I began to observe the aging phenomenon of animals and plants and collect various aging knowledge.

· In 1998, I published a monograph entitled "The Mechanistic Significance and Treatment of Aging" in Beijing Yenching Correspondence Medical College, suggesting that the aging of stem cells in tissues is the cause of individual aging. And from the genetic program theory of aging, it is deduced that in order to run the program, there must be a clock or a "clockwork" device in the nucleus to drive, and the telomere and other multi-copy tandem repeat DNA is the best clockwork candidate, and its copy number reduction is the root cause of stem cell aging. Telomere shortening can only be unidirectional in order to produce the time difference, so telomere length must be reset in germ cells. Furthermore, life has evolved over billions of years with a well-established and redundant defense system, so I conclude that mutated mitochondrial DNA (mtDNA) and cross-linked proteins are not the cause of cell aging, but rather the result of cell aging. In 2010, Ergün Sahin made a similar argument in the journal of Nature: Aging of stem cells in tissues is the cause of aging of individuals, and telomere shortening and mtDNA mutation accumulation are the main causes of aging of stem cells.

· In 2002, I published an article in the Science and Technology Daily titled "Can we Live Forever?" in which I said that in the minds of ordinary people, aging is always stubbornly believed to be a natural law that is irresistible. However, there are many lower animals in nature that can rejuvenate. Therefore, rejuvenation will not violate any laws of nature, and human aging can be conquered. At the same time, I proposed that lysozyme will target to remove mitochondria containing mtDNA mutations which is called mitochondrial autophagy. In a paper published in the journal of Nature Communications on November 14, 2016, a team of researchers from Caltech and UCLA found that fruit flies can selectively clear mitochondria containing mutated mtDNA from their muscles through mitochondrial autophagy.

· Then I went on to publish papers on "Several technological concepts for aging dispel," "The technical conception of repairing stem cell telomeres," "Causes of individual aging," "Individual Aging and Stem Cell Application -- Overturning Traditional Theories and Reveal the Cause of Aging," "Life cycle program driven theory of aging," " The Telomere Age Theory is universal," and "The relationship between ontogenesis and telomeres". These are basically supplements and extensions of the views in 1998, including stem cells, telomeres, and the programmed theory of aging.

· When I learned that some types of cells, whether they will divide or not, will not shorten the telomeres, the cells will still age, and combined with the 2015 paper published by Helen M. Blau at Stanford University, saying that cells with shortened telomeres, through several rounds of hTERT mRNA to lengthen the telomeres, the number of cell divisions is still limited. So, I speculated that in addition to telomeres, there must be another set of telomere-like things in the nucleus that regulate the aging process of cells.

· In 1998, my monograph pointed out that the regulation of cellular aging is multi-copy tandem repeat DNA, and I finally found it, called ribosomal DNA (rDNA). Like telomeres, rDNA is multi-copy tandem repeat DNA. So, in 2021, I published a paper in the journal of Negative (Now renamed "Journal of Air Force Medical University") entitled "Telomere DNA and ribosomal DNA co-regulation model for cell senescence.” I believe that the fundamental cause of cellular aging is caused by the shortening of the telomere and/or rDNA array, which has been verified by experiments, and the aging theory has finally come to an end.