Sorry for the late response, I have apparently been busy posting 24/7 helping others understand the medical and humanitarian miracle that is unfolding...
anywho here's what I have on the potential of epigenetics and specifically apabetalone for anti-aging:

ANTI-AGING

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https://www.cnbc.com/2021/07/17/study-living-past-110-is-becoming-more-likely-longevity-tips.html

“The assumption that the incremental progress in lifestyle and medicine that we’ve seen for the last 200 years or so will continue for the next 80 may be pessimistic given progress in aging biology,” says Andrew Steele, scientist and author of “Ageless: The New Science of Getting Older Without Getting Old.”

“I think there’s the potential for far more exciting breakthroughs by targeting the aging process rather than particular diseases,” he says.

For example, researchers are looking into how to target aging cells called “senescent cells.” Instead of dividing and making new cells, senescent cells hang around and release chemicals and molecules that mess with other healthy cells and trigger inflammation. The number of senescent cells someone has increase as people age, but studies on mice show that they can be removed and potentially increase their lifespans.

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https://www.scientificamerican.com/article/humans-could-live-up-to-150-years-new-research-suggests/

https://www.nia.nih.gov/news/does-cellular-senescence-hold-secrets-healthier-aging

"The number of senescent cells in a person’s body increases with age. As the aging immune system becomes less efficient, senescent cells accumulate and taint healthy cells.

How cellular senescence affects the body

The number of senescent cells in a person’s body increases with age. As the aging immune system becomes less efficient, senescent cells accumulate and taint healthy cells. This can affect a person’s ability to withstand stress or illness; recuperate from injuries; and learn new things, since senescent cells in the brain can degrade cognitive functions.

As a result, cellular senescence has been connected to a multitude of age-related conditions, including cancer, diabetes, osteoporosis, cardiovascular disease, stroke, Alzheimer’s disease and related dementias, and osteoarthritis. It has also been linked to declines in eyesight, mobility, and thinking ability. Investigations are underway to see if senescent skin cells may contribute to sagging and wrinkling, and if senescent cells might also be connected to the cytokine storm of inflammation that makes COVID-19 so deadly for older adults. ...

...For long after that finding, senescence was believed to be just an odd side effect of laboratory cell culture environments. It was poorly understood and studied by only a few research teams, but in the past 20 years, there has been a spike in interest. Today, it is a still young but promising scientific discipline that has sparked more NIH research as well as private industry support for studies to discover and develop drugs that might give Mother Nature a boost in clearing out senescent cells."

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https://www.nature.com/articles/d41586-021-01915-x?utm_source=Nature+Briefing&utm_campaign=eea144dbf8-briefing-dy-20210714&utm_medium=email&utm_term=0_c9dfd39373-eea144dbf8-45366518

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https://www.nature.com/articles/s43587-021-00082-y

The strongest contributor to iAge was the chemokine CXCL9, which was involved in cardiac aging, adverse cardiac remodeling and poor vascular function. Furthermore, aging endothelial cells in human and mice show loss of function, cellular senescence and hallmark phenotypes of arterial stiffness, all of which are reversed by silencing CXCL9. In conclusion, we identify a key role of CXCL9 in age-related chronic inflammation and derive a metric for multimorbidity that can be utilized for the early detection of age-related clinical phenotypes.  Read next article...

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657365/

Macrophages present in the atherosclerotic plaque are largely derived from circulating monocytes infiltrating blood vessels’ walls [7, 75]. In mice, monocytes have been shown to enter into the plaque more readily in the context of diabetes and hypercholesterolemia [76–78]. In non-stimulated conditions, apabetalone suppressed protein secretion of key monocyte chemoattractants MCP-1, MCP-3, GRO-α and IL-8 (87%, 79%, 55% and 32% reduction in DM2 + CVD monocytes, respectively). Apabetalone treatment also potently downregulated the transcription of genes differentially induced by IFNγ in DM2 + CVD monocytes, including the pro-inflammatory cytokine TNF gene (33% reduction), and monocyte chemokine genes CCL7 and CCL8 (90% and 85% reduction, respectively). Additional chemokines that promote chemotaxis and tissue extravasation, CCL2 [62, 64], CXCL9 [79] and CXCL10 [79], were induced by IFNγ in both monocyte populations and were strongly suppressed by apabetalone (91%, 80% and 61% reduction, respectively) (Table ​(Table3).3). BETi treatment is thus predicted to reduce the migratory phenotype of DM2 + CVD monocytes, potentially preventing atherosclerotic plaque infiltration by activated monocytes.

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Apoptosis of Senescent Cells

Apabetalone regulates apoptosis

https://en.m.wikipedia.org/wiki/Apoptosis

            Implication in disease

Defective pathways    

The many different types of apoptotic pathways contain a multitude of different biochemical components, many of them not yet understood.[75] As a pathway is more or less sequential in nature, removing or modifying one component leads to an effect in another. In a living organism, this can have disastrous effects, often in the form of disease or disorder. A discussion of every disease caused by modification of the various apoptotic pathways would be impractical, but the concept overlying each one is the same: The normal functioning of the pathway has been disrupted in such a way as to impair the ability of the cell to undergo normal apoptosis. This results in a cell that lives past its "use-by-date" and is able to replicate and pass on any faulty machinery to its progeny, increasing the likelihood of the cell's becoming cancerous or diseased.

A recently described example of this concept in action can be seen in the development of a lung cancer called NCI-H460.[76] The X-linked inhibitor of apoptosis protein (XIAP) is overexpressed in cells of the H460 cell line. XIAPs bind to the processed form of caspase-9, and suppress the activity of apoptotic activator cytochrome c, therefore overexpression leads to a decrease in the amount of proapoptotic agonists. As a consequence, the balance of anti-apoptotic and proapoptotic effectors is upset in favour of the former, and the damaged cells continue to replicate despite being directed to die. Defects in regulation of apoptosis in cancer cells occur often at the level of control of transcription factors. As a particular example, defects in molecules that control transcription factor NF-κB in cancer change the mode of transcriptional regulation and the response to apoptotic signals, to curtail dependence on the tissue that the cell belongs. This degree of independence from external survival signals, can enable cancer metastasis.[77]

Apabetalone inhibits NF-kB

https://clinicalepigeneticsjournal.biomedcentral.com/articles/10.1186/s13148-019-0696-z

Page 42:  https://docs.wixstatic.com/ugd/5a7874_570507cfb9564baa8f4380915735e21b.pdf
Essential to the unique properties of senescent cells is the Senescence-Associated Secretory Phenotype (SASP). The SASP is comprised of numerous chemokines, growth factors, cytokines, matrix metalloproteinases and small molecular weight metabolites. This change in inflammatory signaling spreads to other cells in the area, hastening their own decline into an aging state, and further accelerating the overall aging of the organism. Notably, this SASP has been shown to drive atherosclerosis at all stages. As well, the SASP has been shown to be deeply involved in CVD in general, in addition to diabetes, Alzheimer’s disease and CKD. Unsurprisingly, elimination of senescent cells for treatment of disease and of retarding or even reversing the aging process is currently a hot topic. Apabetalone shows promise in this area.

A small molecule medicine will be needed to activate receptors of osteocalcin
https://www.theguardian.com/science/2020/jul/04/does-the-key-to-anti-ageing-lie-in-our-bones

That's it for now!!  Peace!