Anthony Lagnado
Newcastle University
DNA damageTelomereFibrosisSenescenceBiology
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Publications 14
#1Brittany A Eckhardt (Mayo Clinic)H-Index: 1
#2Jennifer L Rowsey (Mayo Clinic)H-Index: 1
Last. Kuntol Rakshit (Mayo Clinic)H-Index: 11
view all 17 authors...
The worldwide prevalence of type 2 diabetes (T2D) is increasing. Despite normal to higher bone density, patients with T2D paradoxically have elevated fracture risk resulting, in part, from poor bone quality. Advanced glycation endproducts (AGEs) and inflammation as a consequence of enhanced receptor for AGE (RAGE) signaling are hypothesized culprits, although the exact mechanisms underlying skeletal dysfunction in T2D are unclear. Lack of inducible models that permit environmental (in obesity) a...
#1Anthony LagnadoH-Index: 3
#2Stella VictorelliH-Index: 4
Last. João F. PassosH-Index: 29
view all 3 authors...
#1Abhishek Chandra (UR: University of Rochester)H-Index: 4
#2Anthony Lagnado (Mayo Clinic)H-Index: 3
Last. João F. Passos (Mayo Clinic)H-Index: 29
view all 11 authors...
Clinical radiotherapy treats life-threatening cancers, but the radiation often affects neighboring normal tissues including bone. Acute effects of ionizing radiation include oxidative stress, DNA damage, and cellular apoptosis. We show in this study that a large proportion of bone marrow cells, osteoblasts, and matrix-embedded osteocytes recover from these insults only to attain a senescent profile. Bone analyses of senescence-associated genes, senescence-associated beta-galactosidase (SA-beta-g...
1 CitationsSource
#2Tianhui LiuH-Index: 1
Last. Xue LeiH-Index: 1
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Cellular senescence is a potent tumor suppressor mechanism but also contributes to aging and aging-related diseases. Senescence is characterized by a stable cell cycle arrest and a complex proinflammatory secretome, termed the senescence-associated secretory phenotype (SASP). We recently discovered that cytoplasmic chromatin fragments (CCFs), extruded from the nucleus of senescent cells, trigger the SASP through activation of the innate immunity cytosolic DNA sensing cGAS-STING pathway. However,...
4 CitationsSource
#1LaTonya J. Hickson (Mayo Clinic)H-Index: 16
#2Larissa Prata (Mayo Clinic)H-Index: 3
Last. Kyra L. Jordan (Mayo Clinic)H-Index: 15
view all 38 authors...
2 CitationsSource
#1Abhishek ChandraH-Index: 4
#2Anthony LagnadoH-Index: 3
view all 11 authors...
#1Andrew R.J. Young (University of Cambridge)H-Index: 15
#2Liam D. Cassidy (University of Cambridge)H-Index: 6
Last. Masashi Narita (University of Cambridge)H-Index: 36
view all 15 authors...
Autophagy is an important cellular degradation pathway with a central role in metabolism as well as basic quality control, two processes inextricably linked to ageing. A decrease in autophagy is associated with increasing age, yet it is unknown if this is causal in the ageing process, and whether autophagy restoration can counteract these ageing effects. Here we demonstrate that systemic autophagy inhibition induces the premature acquisition of age-associated phenotypes and pathologies in mammal...
2 CitationsSource
#1Stella Victorelli (Newcastle University)H-Index: 4
#2Anthony Lagnado (Newcastle University)H-Index: 3
Last. João F. Passos (Newcastle University)H-Index: 29
view all 18 authors...
Cellular senescence has been shown to contribute to skin ageing. However, the role of melanocytes in the process is understudied. Our data show that melanocytes are the only epidermal cell type to express the senescence marker p16(INK4A) during human skin ageing. Aged melanocytes also display additional markers of senescence such as reduced HMGB1 and dysfunctional telomeres, without detectable telomere shortening. Additionally, senescent melanocyte SASP induces telomere dysfunction in paracrine ...
2 CitationsSource
#1LaTonya J. Hickson (Mayo Clinic)H-Index: 16
#2Larissa Prata (Mayo Clinic)H-Index: 3
Last. James L. KirklandH-Index: 55
view all 33 authors...
Abstract Background Senescent cells, which can release factors that cause inflammation and dysfunction, the senescence-associated secretory phenotype (SASP), accumulate with ageing and at etiological sites in multiple chronic diseases. Senolytics, including the combination of Dasatinib and Quercetin (D + Q), selectively eliminate senescent cells by transiently disabling pro-survival networks that defend them against their own apoptotic environment. In the first clinical trial of senolytics, D + ...
20 CitationsSource
#1Rhys Anderson (Newcastle University)H-Index: 7
#2Anthony Lagnado (Newcastle University)H-Index: 3
Last. João F. Passos (Newcastle University)H-Index: 29
view all 34 authors...
Abstract Ageing is the biggest risk factor for cardiovascular disease. Cellular senescence, a process driven in part by telomere shortening, has been implicated in age‐related tissue dysfunction. Here, we address the question of how senescence is induced in rarely dividing/post‐mitotic cardiomyocytes and investigate whether clearance of senescent cells attenuates age‐related cardiac dysfunction. During ageing, human and murine cardiomyocytes acquire a senescent‐like phenotype characterised by pe...
16 CitationsSource