Using an epigenetic clock to distinguish cellular aging from senescence

The 2016 UK/UCLA human study found: “Induction of replicative senescence (RS) and oncogene-induced senescence (OIS) are accompanied by ageing of the cell. However, senescence induced by DNA damage is not, even though RS and OIS activate the cellular DNA damage response pathway, highlighting the independence of senescence from cellular ageing. We used primary endothelial cells … Continue reading Using an epigenetic clock to distinguish cellular aging from senescence

Epigenetic mechanisms regulate bone growth

This 2017 Baltimore/China rodent study found: “MSPC [Mesenchymal stem/progenitor cell] senescence is epigenetically controlled by the polycomb histone methyltransferase enhancer of zeste homolog 2 (Ezh2) and its trimethylation of histone H3 on Lysine 27 (H3K27me3) mark. Ezh2 maintains the repression of key cell senescence inducer genes through H3K27me3. Our work establishes the role of Ezh2-H3K27me3 … Continue reading Epigenetic mechanisms regulate bone growth

Epigenetic effects of cruciferous vegetable compounds

This 2017 German review discussed the results of many of the studies performed over the past thirty years investigating the health-promoting effects of cruciferous vegetable compounds: “SFN [sulforaphane] [is] the ITC [isothiocyanate] that is the most extensively studied for its chemopreventive and anti-inflammatory properties in vitro, as well as in vivo. Due to the reversible … Continue reading Epigenetic effects of cruciferous vegetable compounds

Lack of oxygen’s epigenetic effects

This 2016 Finnish review’s subject was the epigenetic effects of hypoxia: “Ever since the Cambrian period, oxygen availability has been in the center of energy metabolism. Hypoxia stabilizes the expression of hypoxia-inducible transcription factor-1α (HIF-1α), which controls the expression of hundreds of survival genes related to enhanced energy metabolism and autophagy. There are several other … Continue reading Lack of oxygen’s epigenetic effects

The current paradigm of child abuse limits pre-childhood causal research

As an adult, what would be your primary concern if you suspected that your early life had something to do with current problems? Would you be interested in effective treatments of causes of your symptoms? Such information wasn’t available in this 2016 Miami review of the effects of child abuse. The review laid out the … Continue reading The current paradigm of child abuse limits pre-childhood causal research

Using an epigenetic clock with older adults

This 2016 German human study found: “Epigenetic age acceleration is correlated with clinically relevant aging-related phenotypes through pathways unrelated to cellular senescence as assessed by telomere length. The current work employed the frailty index, a multi-dimensional approach that combines [34] parameters of multiple physiological systems and functional capacities. The present findings were based on [1,820] … Continue reading Using an epigenetic clock with older adults

Using an epigenetic clock with children

This 2015 UK human study by many of the coauthors of What’s the origin of the problem of being fat? applied the Horvath epigenetic clock method to the same UK mother-child pairs and a Danish cohort: “There has been no investigation on prenatal and antenatal factors that affect AA [age acceleration] in children. It is … Continue reading Using an epigenetic clock with children

The link between scientific value and content is broken at PNAS.org

Should we expect content posted on the Proceedings of the National Academy of Sciences of the United States of America to have scientific value? This 2016 Singapore study was a “PNAS Direct Submission” that claimed: “This paper makes a singular contribution to understanding the association between biological aging indexed by leukocyte telomeres length (LTL) and … Continue reading The link between scientific value and content is broken at PNAS.org

Telomerase activity outside of telomere maintenance

This 2016 Singapore review was on the role of telomerase in cancers. From its background section: “Telomeres are conserved, repetitive sequences located at the ends of eukaryotic chromosomes which protect the integrity of genomic DNA. DNA polymerase is unable to replicate the 5′ [carbon number] ends of chromosomes, hence, cells require a RNA dependent DNA … Continue reading Telomerase activity outside of telomere maintenance

DNA damage to fat cells may cause obesity and insulin resistance

This 2015 Indiana rodent study found: “DNA damage is a root cause of adipocyte senescence [fat cells that can no longer replicate], which plays a determining role in the development of obesity and insulin resistance.” The researchers removed the capability for the subject mice to produce a protein that “plays an essential role in preventing … Continue reading DNA damage to fat cells may cause obesity and insulin resistance