Area of research
Physiology · Aging
Research interest
Research interests include Telomeres, Telomerase, and Senescence, Genetics, Aging, and Longevity in Model Organisms, Neutrophil, Myeloperoxidase and Oxidative Mechanisms, and Mitochondrial Function and Pathology.
Tomatidine is a senotherapeutic compound that improves cognitive function and reduces cellular senescence in aged mice.
Roadmap for alleviating the manifestations of ageing in the cardiovascular system
Advancing biological understanding of cellular senescence with computational multiomics
p53 enhances DNA repair and suppresses cytoplasmic chromatin fragments and inflammation in senescent cells.
Senescent cell transplantation into the skin induces age-related peripheral dysfunction and cognitive decline.
Mitochondrial RNA cytosolic leakage drives the SASP.
Advancing biological understanding of cellular senescence with computational multiomics.
Cytosolic DNA crosstalk in senescence: a new axis of inflammatory signaling?
Distinct senotypes in p16- and p21-positive cells across human and mouse aging tissues.
Inactivation of Histone Chaperone HIRA Unmasks a Link Between Normal Embryonic Development of Melanoblasts and Maintenance of Adult Melanocyte Stem Cells.
SenNet recommendations for detecting senescent cells in different tissues
Guidelines for minimal information on cellular senescence experimentation in vivo
Guidelines for minimal information on cellular senescence experimentation in vivo.
Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity
Osteochondroprogenitor cells and neutrophils expressing p21 and senescence markers modulate fracture repair
Author Correction: Apoptotic stress causes mtDNA release during senescence and drives the SASP.
Determining the feasibility of characterising cellular senescence in human skeletal muscle and exploring associations with muscle morphology and physical function at different ages: findings from the MASS_Lifecourse Study.
Telomere dysfunction in chronic liver disease: The link from aging.
Mitochondrial RNA cytosolic leakage drives the SASP
Mitochondrial metabolism and epigenetic crosstalk drive the SASP
Osteochondroprogenitor cells and neutrophils expressing p21 and senescence markers modulate fracture repair
Apoptotic stress causes mtDNA release during senescence and drives the SASP
Apoptotic stress causes mtDNA release during senescence and drives the SASP.
Cellular senescence: all roads lead to mitochondria.
Spatial mapping of cellular senescence: emerging challenges and opportunities
Spatial mapping of cellular senescence: emerging challenges and opportunities.
Local senolysis in aged mice only partially replicates the benefits of systemic senolysis
3D bioprinting-a model for skin aging.
New Horizons in cellular senescence for clinicians.
A chronic wound model to investigate skin cellular senescence.