Sirt1 & Metformin some of the older tweets collected

NEW Metformin inhibits the senescence-associated secretory phenotype by interfering with IKK/NF-κB activation http://t.co/5ctKfJjY6k

— Wiley Genetics (@WileyGenetics) April 23, 2013

Metformin lowers the threshold for stress-induced senescence: a role for the microRNA-200 family and miR-205.http://t.co/hDs4p28T

— anamika mehta (@anamika13) October 3, 2012

NEVER !

Sirt1 More

Perspectives on translational and therapeutic aspects of SIRT1 in inflammaging and senescence. http://t.co/NpCeFcrZCC

— Kelly A. Hogan Ph.D. (@Loose_Lab_Rat) June 17, 2014

PPARδ-mediated inhibition of angiotensin II-induced premature senescence in endothelial cells is SIRT1-dependent. http://t.co/pSRZjvBfEs

— Kelly A. Hogan Ph.D. (@Loose_Lab_Rat) June 17, 2014

Father's Day 2014

------- *EDIT* & Phillies broadcaster Tom McCarthy caught a home run while on air (and threw it back)

Accelerated senescence of cord blood endothelial progenitor cells in premature neonates is driven by SIRT1 decreased expression.

Epidemiological and experimental studies indicate that early vascular dysfunction occurs in low-birth-weight subjects, especially preterm (PT) infants. We recently reported impaired angiogenic activity of endothelial colony-forming cells (ECFCs) in this condition. We hypothesized that ECFC dysfunction in PT might result from premature senescence and investigated the underlying mechanisms. Compared with ECFCs from term neonates (n = 18), ECFCs isolated from PT (n = 29) display an accelerated senescence sustained by growth arrest and increased senescence-associated β-galactosidase activity. Increased p16(INK4a) expression, in the absence of telomere shortening, indicates that premature PT-ECFC aging results from stress-induced senescence. SIRT1 level, a nicotinamide adenine dinucleotide-dependent deacetylase with anti-aging activities, is dramatically decreased in PT-ECFCs and correlated with gestational age. SIRT1 deficiency is subsequent to epigenetic silencing of its promoter. Transient SIRT1 overexpression or chemical induction by resveratrol treatment reverses senescence phenotype, and rescues in vitro PT-ECFC angiogenic defect in a SIRT1-dependent manner. SIRT1 overexpression also restores PT-ECFC capacity for neovessel formation in vivo. We thus demonstrate that decreased expression of SIRT1 drives accelerated senescence of PT-ECFCs, and acts as a critical determinant of the PT-ECFC angiogenic defect. These findings lay new grounds for understanding the increased cardiovascular risk in individuals born prematurely and open perspectives for therapeutic strategy.
http://www.ncbi.nlm.nih.gov/pubmed/24518759

Sirt1: A protein required for integrity of induced pluripotent stem cells

A study published today in the journal Stem Cell Reports, from the Cell Publishing Group, reveals that the SIRT1 protein is needed to lengthen and maintain telomeres during cell reprogramming. SIRT1 also guarantees the integrity of the genome of stem cells that come out of the cell reprogramming process; these cells are known as iPS cells (induced Pluripotent Stem cells). Read more at: http://phys.org/news/2014-04-protein-required-pluripotent-stem-cells.html#jCp
http://phys.org/news/2014-04-protein-required-pluripotent-stem-cells.html#inlRlv