João F. Passos
Newcastle University
TelomereAgeingSenescenceBiologyCell biology
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Publications 103
#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...
#1Emily Dookun (Newcastle University)H-Index: 3
#2Anna WalaszczykH-Index: 2
Last. Eleanor K Gill ('QUB': Queen's University Belfast)H-Index: 1
view all 20 authors...
Rationale: A key component of cardiac ischemia-reperfusion injury (IRI) is the increased generation of reactive oxygen species, leading to enhanced inflammation and tissue dysfunction in patients following intervention for myocardial infarction. We have previously shown that oxidative stress induces myocardial senescence, promoting adverse myocardial remodeling and cardiac dysfunction via the expression of a proinflammatory senescence-associated secretory phenotype (SASP). In this study we hypot...
#1Robert J. Pignolo (Mayo Clinic)H-Index: 31
#2João F. Passos (Mayo Clinic)H-Index: 29
Last. James L. Kirkland (Mayo Clinic)H-Index: 55
view all 5 authors...
Cellular senescence is a primary aging process and tumor suppressive mechanism characterized by irreversible growth arrest, apoptosis resistance, production of a senescence-associated secretory phenotype (SASP), mitochondrial dysfunction, and alterations in DNA and chromatin. In preclinical aging models, accumulation of senescent cells is associated with multiple chronic diseases and disorders, geriatric syndromes, multimorbidity, and accelerated aging phenotypes. In animals, genetic and pharmac...
#1Stella Victorelli (Mayo Clinic)H-Index: 4
#2João F. Passos (Mayo Clinic)H-Index: 29
ABSTRACTCellular senescence is an irreversible cell cycle arrest, which can be triggered by a number of stressors, including telomere damage. Among many other phenotypic changes, senescence is acco...
#1Abhishek Chandra (UR: University of Rochester)H-Index: 4
#2Anthony Lagnado (Mayo Clinic)H-Index: 3
Last. João F. Passos (UR: University of Rochester)
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