Laura J. Niedernhofer

NF-κB inhibition delays DNA damage-induced senescence and aging in mice.

DNA damage triggers a chronic autoinflammatory response, leading to fat depletion in NER progeria.

Investigating the role of DNA damage in tobacco smoking-induced spine degeneration.

Pharmacologic IKK/NF-κB inhibition causes antigen presenting cells to undergo TNFα dependent ROS-mediated programmed cell death.

Comparison of mice with accelerated aging caused by distinct mechanisms.

NF-κB activation with aging: characterization and therapeutic inhibition.

The Achilles' heel of senescent cells: from transcriptome to senolytic drugs.

In vivo detection and replication studies of α-anomeric lesions of 2'-deoxyribonucleosides.

Identification of a novel senolytic agent, navitoclax, targeting the Bcl-2 family of anti-apoptotic factors.

Barriers to the Preclinical Development of Therapeutics that Target Aging Mechanisms.

Smartphone Analytics: Mobilizing the Lab into the Cloud for Omic-Scale Analyses.

mTOR signaling plays a critical role in the defects observed in muscle-derived stem/progenitor cells isolated from a murine model of accelerated aging.

Molecular pathology endpoints useful for aging studies.

Occurrence, Biological Consequences, and Human Health Relevance of Oxidative Stress-Induced DNA Damage.

Quantitative Analysis of Cellular Senescence in Culture and In Vivo.

Expansion of myeloid-derived suppressor cells with aging in the bone marrow of mice through a NF-κB-dependent mechanism.

New agents that target senescent cells: the flavone, fisetin, and the BCL-X inhibitors, A1331852 and A1155463.

Systems biology guided by XCMS Online metabolomics.

ADAMTS5 Deficiency Protects Mice From Chronic Tobacco Smoking-induced Intervertebral Disc Degeneration.

Advances in Therapeutic Approaches to Extend Healthspan: a perspective from the 2 Scripps Symposium on the Biology of Aging.

Inhibition of NF-κB improves the stress resistance and myogenic differentiation of MDSPCs isolated from naturally aged mice.

Senescent intervertebral disc cells exhibit perturbed matrix homeostasis phenotype.

The Clinical Potential of Senolytic Drugs.

Identification of HSP90 inhibitors as a novel class of senolytics.

ERCC4 variants identified in a cohort of patients with segmental progeroid syndromes.

Circulating levels of monocyte chemoattractant protein-1 as a potential measure of biological age in mice and frailty in humans.

Oxidation Products of 5-Methylcytosine are Decreased in Senescent Cells and Tissues of Progeroid Mice.

Senotherapeutics for healthy ageing.

Spontaneous DNA damage to the nuclear genome promotes senescence, redox imbalance and aging.

ERCC1-deficient cells and mice are hypersensitive to lipid peroxidation.

Hsp90 inhibitors as senolytic drugs to extend healthy aging.

Development of novel NEMO-binding domain mimetics for inhibiting IKK/NF-κB activation.

Neurodegeneration as the presenting symptom in 2 adults with xeroderma pigmentosum complementation group F.

Nuclear Genomic Instability and Aging.

Senolytics improve physical function and increase lifespan in old age.

Dysregulation of DAF-16/FOXO3A-mediated stress responses accelerates oxidative DNA damage induced aging.

Fisetin is a senotherapeutic that extends health and lifespan.

Mouse Models of Accelerated Cellular Senescence.

Methods to Quantify the NF-κB Pathway During Senescence.

Measuring biological age in mice using differential mass spectrometry.

Adenoviral gene transfer of a single-chain IL-23 induces psoriatic arthritis-like symptoms in NOD mice.