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Belosludtsev, K., Saris, N.E., Andersson, L.C., Belosludtseva, N., Agafonov, A., Sharma, A., Moshkov, D.A. and Mironova, G.D. (2006) On the Mechanism of Palmitic Acid-Induced Apoptosis: The Role of a Pore Induced by Palmitic Acid and Ca2+ in Mitochondria. Journal of Bioenergetics and Biomembranes, 38, 113-120.
http://dx.doi.org/10.1007/s10863-006-9010-9

has been cited by the following article:

• TITLE: Anti-Aging Genes Improve Appetite Regulation and Reverse Cell Senescence and Apoptosis in Global Populations

  AUTHORS: Ian James Martins

  KEYWORDS: Anti-Aging Genes, Appetite, Environment, Nutrition, Senescence

  JOURNAL NAME: Advances in Aging Research, Vol.5 No.1, January 28, 2016

  ABSTRACT: Appetite regulation by nutritional intervention is required early in life that involves the anti-aging gene Sirtuin 1 (Sirt 1) with Sirt 1 maintenance of other cellular anti-aging genes involved in cell circadian rhythm, senescence and apoptosis. Interests in anti-aging therapy with appetite regulation improve an individual’s survival to metabolic disease induced by gene-environment interactions by maintenance of the anti-aging genes connected to the metabolism of bacterial lipopolysaccharides, drugs and xenobiotics. Interventions to the aging process involve early calorie restriction with appetite regulation connected to appropriate genetic mechanisms that involve mitochondrial biogenesis and DNA repair in neurons. In the aging process as the anti-aging genes are suppressed as a result of transcriptional dysregulation chronic disease accelerations and connected to insulin resistance, non-alcoholic fatty liver disease (NAFLD) and neurodegenerative diseases such as Parkinson’s disease and Alzheimer’s disease. Interests in the gene-environment interaction indicate that the anti-aging gene Sirt 1that regulates food intake has been repressed early in the aging process in various global populations. The connections between Sirt 1 and other anti-aging genes such as Klotho, p66Shc (longevity protein) and Forkhead box proteins (FOXO1/ FOXO3a) have been associated with programmed cell death and alterations in these anti-aging genesregulate glucose, lipid and amyloid beta metabolism that are important to various chronic diseases.