‘Incredible’ gene-editing result in mice inspires plans to treat premature-aging syndrome in children

Science ◽  
2021 ◽  
Author(s):  
Jocelyn Kaiser
Keyword(s):  
Gene Editing ◽  
Premature Aging ◽  
Premature Aging Syndrome

scholarly journals Podiatric complications during a premature aging syndrome: Rare case

2016 ◽  
Vol 59 ◽  
pp. e28-e29
Author(s):  
Siham Zahi ◽  
Laila Mahir ◽  
Soumia Meftah ◽  
Fatima Lmidmani ◽  
Abdellatif El fatimi
Keyword(s):  
Rare Case ◽  
Premature Aging ◽  
Premature Aging Syndrome

scholarly journals LMNA ‐associated cardiocutaneous progeria: An inherited autosomal dominant premature aging syndrome with late onset

2013 ◽  
Vol 161 (7) ◽  
pp. 1599-1611 ◽  
Author(s):  
Megan S. Kane ◽  
Mark E. Lindsay ◽  
Daniel P. Judge ◽  
Jemima Barrowman ◽  
Colette Ap Rhys ◽  
...  
Keyword(s):  
Autosomal Dominant ◽  
Late Onset ◽  
Premature Aging ◽  
Premature Aging Syndrome

scholarly journals LMNA-mutated Rabbits: A Model of Premature Aging Syndrome with Muscular Dystrophy and Dilated Cardiomyopathy

2019 ◽  
Vol 10 (1) ◽  
pp. 102 ◽  
Author(s):  
Tingting Sui ◽  
Di Liu ◽  
Tingjun Liu ◽  
Jichao Deng ◽  
Mao Chen ◽  
...  
Keyword(s):  
Muscular Dystrophy ◽  
Dilated Cardiomyopathy ◽  
Premature Aging ◽  
Premature Aging Syndrome

Telomere length and type 2 diabetes in males, a premature aging syndrome

2011 ◽  
Vol 15 (1) ◽  
pp. 54-58 ◽  
Author(s):  
Blanca Murillo-Ortiz ◽  
Froylán Albarrán-Tamayo ◽  
Diego Arenas-Aranda ◽  
Luis Benítez-Bribiesca ◽  
JM Malacara-Hernández ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Telomere Length ◽  
Premature Aging ◽  
Premature Aging Syndrome

scholarly journals Lamin B1 fluctuations have differential effects on cellular proliferation and senescence

2013 ◽  
Vol 200 (5) ◽  
pp. 605-617 ◽  
Author(s):  
Oliver Dreesen ◽  
Alexandre Chojnowski ◽  
Peh Fern Ong ◽  
Tian Yun Zhao ◽  
John E. Common ◽  
...  
Keyword(s):  
Cellular Proliferation ◽  
Nuclear Lamina ◽  
Dermal Fibroblasts ◽  
Premature Aging ◽  
Simultaneous Reduction ◽  
Messenger Ribonucleic Acid ◽  
Rna Translation ◽  
Protein Levels ◽  
Lamin B1 ◽  
Premature Aging Syndrome

The nuclear lamina consists of A- and B-type lamins. Mutations in LMNA cause many human diseases, including progeria, a premature aging syndrome, whereas LMNB1 duplication causes adult-onset autosomal dominant leukodystrophy (ADLD). LMNB1 is reduced in cells from progeria patients, but the significance of this reduction is unclear. In this paper, we show that LMNB1 protein levels decline in senescent human dermal fibroblasts and keratinocytes, mediated by reduced transcription and inhibition of LMNB1 messenger ribonucleic acid (RNA) translation by miRNA-23a. This reduction is also observed in chronologically aged human skin tissue. To determine whether altered LMNB1 levels cause senescence, we either increased or reduced LMNB1. Both LMNB1 depletion and overexpression inhibited proliferation, but only LMNB1 overexpression induced senescence, which was prevented by telomerase expression or inactivation of p53. This phenotype was exacerbated by a simultaneous reduction of LMNA/C. Our results demonstrate that altering LMNB1 levels inhibits proliferation and are relevant to understanding the molecular pathology of ADLD.

scholarly journals Molecular Mechanisms Underlying Accelerated Aging by Defects in the FGF23-Klotho System

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Makoto Kuro-o
Keyword(s):  
Molecular Mechanisms ◽  
Accelerated Aging ◽  
Basic Research ◽  
Cellular Level ◽  
Premature Aging ◽  
Health Span ◽  
Aging Society ◽  
Age Related ◽  
Evolutionarily Conserved ◽  
Premature Aging Syndrome

The basic research of aging has been primarily focused on elucidating mechanisms of aging and longevity that are evolutionarily conserved from yeasts to primates. Such efforts have culminated in the notion that (1) senescence at the cellular level is associated with aging at the organismal level and that (2) calorie restriction and growth suppression decelerate aging. However, these important findings in the basic research have not necessarily been linked to improvement of daily medical practice in the aging society. It has become increasingly important to investigate mechanisms of aging unique to mammals or humans and apply the research fruits for the treatment of major age-related disorders to extend the health span. Seminal studies on the klotho mouse, a mutant exhibiting a premature aging syndrome, have identified phosphate as a proaging factor in mammals. In this review, mechanisms of phosphate-induced premature aging and potential therapeutic targets will be discussed, which may be directly applicable for developing novel strategies for the treatment of chronic kidney disease and its complications.

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