A5068519051- Telomeres, Telomerase, and Senescence
- Genetics, Aging, and Longevity in Model Organisms
- Circadian rhythm and melatonin
- Neutrophil, Myeloperoxidase and Oxidative Mechanisms
- Single-cell and spatial transcriptomics
- Skin Protection and Aging
- MicroRNA in disease regulation
- Adipose Tissue and Metabolism
- Autophagy in Disease and Therapy
- Wound Healing and Treatments
- Muscle Physiology and Disorders
- Antimicrobial Peptides and Activities
- Adipokines, Inflammation, and Metabolic Diseases
- melanin and skin pigmentation
- Mesenchymal stem cell research
- Neuroinflammation and Neurodegeneration Mechanisms
- Regulation of Appetite and Obesity
- CRISPR and Genetic Engineering
- Atherosclerosis and Cardiovascular Diseases
- Silk-based biomaterials and applications
- Circular RNAs in diseases
- Dietary Effects on Health
- Pressure Ulcer Prevention and Management
- Calcium signaling and nucleotide metabolism
- Planarian Biology and Electrostimulation
Ludwig Boltzmann Institute for Experimental and Clinical Traumatology
2021-2025
Austrian Cluster for Tissue Regeneration
2021-2025
Ludwig Boltzmann Institute for Digital Health and Prevention
2021-2025
Ludwig Boltzmann Gesellschaft
2021-2024
Mayo Clinic in Florida
2016-2022
Newcastle University
2015-2019
Newcastle Hospitals - Campus for Ageing and Vitality
2017-2019
Mayo Clinic
2015-2019
WinnMed
2019
Polish Academy of Sciences
2018
Abstract The incidence of non-alcoholic fatty liver disease (NAFLD) increases with age. Cellular senescence refers to a state irreversible cell-cycle arrest combined the secretion proinflammatory cytokines and mitochondrial dysfunction. Senescent cells contribute age-related tissue degeneration. Here we show that accumulation senescent promotes hepatic fat steatosis. We report close correlation between markers hepatocyte senescence. elimination by suicide gene-meditated ablation p16 Ink4a...
Significance A hallmark of aging is chronic sterile inflammation, which closely associated with frailty and age-related diseases. We found that senescent fat progenitor cells accumulate in adipose tissue acquire a senescence-associated secretory phenotype (SASP), increased production proinflammatory cytokines compared nonsenescent cells. These provoked inflammation induced macrophage migration. The JAK pathway activated aging, the SASP can be suppressed by inhibiting JAK1/2 inhibitors...
While reports suggest a single dose of senolytics may improve vasomotor function, the structural and functional impact long-term senolytic treatment is unknown. To determine whether improves vascular stiffness, intimal plaque size composition in aged or hypercholesterolemic mice with established disease. Senolytic (intermittent Dasatinib + Quercetin via oral gavage) resulted significant reductions senescent cell markers (TAF+ cells) medial layer aorta from mice, but not atherosclerotic...
Adipose tissue inflammation and dysfunction are associated with obesity-related insulin resistance diabetes, but mechanisms underlying this relationship unclear. Although senescent cells accumulate in adipose of obese humans rodents, a direct pathogenic role for these the development diabetes remains to be demonstrated. Here, we show that reducing cell burden mice, either by activating drug-inducible "suicide" genes driven p16
ABSTRACT Cellular senescence is a fundamental mechanism by which cells remain metabolically active yet cease dividing and undergo distinct phenotypic alterations, including upregulation of p16Ink4a, profound secretome changes, telomere shortening, decondensation pericentromeric satellite DNA. Because senescent accumulate in multiple tissues with aging, these the dysfunctional factors they secrete, termed senescence-associated secretory phenotype (SASP), are increasingly recognized as...
Cellular senescence entails a stable cell-cycle arrest and pro-inflammatory secretory phenotype, which contributes to aging age-related diseases. Obesity is associated with increased senescent cell burden neuropsychiatric disorders, including anxiety depression. To investigate the role of in obesity-related dysfunction, we used INK-ATTAC mouse model, from p16
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Osteoarthritis (OA) is the leading form of arthritis in elderly, causing pain, disability, and immobility. OA has been associated with accumulation senescent cells or near joints. However, evidence for a causal link between cellular senescence lacking. Here, we present novel cell transplantation model involving injection small numbers nonsenescent from ear cartilage luciferase-expressing mice into knee joint area wild-type mice. By using bioluminescence 18FDG PET imaging, could track...
Abstract Cellular senescence is characterized by an irreversible cell cycle arrest and a pro‐inflammatory senescence‐associated secretory phenotype (SASP), which major contributor to aging age‐related diseases. Clearance of senescent cells has been shown improve brain function in mouse models neurodegenerative However, it still unknown whether clearance alleviates cognitive dysfunction during the process. To investigate this, we first conducted single‐nuclei single‐cell RNA‐seq hippocampus...
Abstract Senescent cells accumulate with age in multiple tissues and may cause age‐associated disease functional decline. In vitro, senescent induce senescence bystander cells. To see how important this effect be for accumulation of vivo, we xenotransplanted into skeletal muscle skin immunocompromised NSG mice. 3 weeks after the last transplantation, mouse dermal fibroblasts myofibres displayed markers vicinity transplanted cells, but not where non‐senescent or no were injected. Adjacent to...
Article25 March 2021Open Access Source DataTransparent process Neutrophils induce paracrine telomere dysfunction and senescence in ROS-dependent manner Anthony Lagnado Department of Physiology Biomedical Engineering, Mayo Clinic, Rochester, MN, USA Robert Arlene Kogod Center on Aging, Search for more papers by this author Jack Leslie Newcastle Fibrosis Research Group, Biosciences Institute, University, upon Tyne, UK Marie-Helene Ruchaud-Sparagano Translational Stella Victorelli Petra Hirsova...
Abstract Cellular senescence is a plausible mediator of inflammation-related tissue dysfunction. In the aged brain, senescent cell identities and mechanisms by which they exert adverse influence are unclear. Here we used high-dimensional molecular profiling, coupled with mechanistic experiments, to study properties cells in mouse brain. We show that inflammatory expression profiles increase age brain region- sex-specific. p16 -positive myeloid exhibiting disease-associated activation...
Significance We show, for the first time to our knowledge, that vimentin intermediate filaments establish mitotic polarity in dividing mammalian cell lines. By confining damaged, misfolded, and aggregated proteins JUNQ inclusion bodies, mediates their asymmetric partitioning during division. also, provide direct evidence of active proteasomal degradation dynamic bodies. This work sheds light on an important rejuvenation mechanism cells provides new biological insight into role bodies...
SQSTM1/p62 (sequestosome 1) selectively targets polyubiquitinated proteins for degradation via macroautophagy and the proteasome. Additionally, SQSTM1 shuttles between cytoplasmic nuclear compartments, although its role in nucleus is relatively unknown. Here, we report that dynamically associates with DNA damage foci (DDF) regulates repair. Upon induction of interacts FLNA (filamin A), which has previously been shown to recruit repair protein RAD51 (RAD51 recombinase) double-strand breaks...