01 / RESEARCH AREAS
Mechanisms of aging
The biology beneath the passing years. From cellular change to the whole organism.
QUESTIONS WE WANT TO UNDERSTAND
Which changes drive aging, and which accompany it?
How do processes at different biological scales interact?
When does a mechanism found in a model apply to humans?
These questions describe the scope of this area. They are not findings or a list of active studies.
Research in this area
Newest published first
1–12 of 29 articles
Does a Younger “Vascular Age” Mean Improved Vascular Structure?
Vascular readings can carry health information, but a lower predicted age, a changed arterial wall, and fewer future clinical events are separate results. We reanalyzed a public dataset of 36,223…
- Cross-sectional age and algorithmsModerate
- Pressure and mechanical conditionsStrong
- Acute human tone and vessel sitesLimited
- Clinical prognosisModerate
- Management trial and surrogacyNot yet determinable
How Much Can Enhanced DNA Repair Explain Longevity Differences Between Species?
Bowhead-whale cell experiments give genome maintenance experimental support as one explanation of exceptional longevity. Several repair reporters, survival after damage and mutation outcomes favor…
- Selected cross-species cell maintenanceModerate
- Conditional locus error spectraLimited
- CIRBP cellular perturbationModerate
- Female fly survival and whole-organism tradeoffsLimited
- Whale lifespan attribution and human benefitNot yet determinable
Protein accumulation in the aging brain: made locally or acquired from other cells?
Mouse experiments support the presence of neuron-derived protein material in microglia, with higher associated labeling signals in aged microglial samples. Some labeled proteins also disappear more…
- Mouse cellular origin and recipient materialModerate
- Effective persistence in selected brain regionsModerate
- Routes, intrinsic rates and functional attributionLimited
- Normal-human aging and intervention benefitNot yet determinable
Matrix fragments: drivers of aging, or echoes of tissue injury?
Elastin fragments can participate in immune signaling, and mouse interventions provide causal clues. Higher circulating concentrations can also reflect tissue injury, increased release or slower…
- Circulating levels and originsLimited
- Animal signaling mechanismsModerate
- Naturally aged lifespanLimited
- Specificity and safetyLimited
- Human causality and healthspanNot yet determinable
Hepatic immune signals: new T cells, or expansion of existing cells?
A mouse study temporarily supplied three immune-support signals from the liver and improved some vaccine and antitumor responses in aged animals. Evidence for thymic involvement matters, but larger…
- Thymus-related processesModerate
- Repertoire depth and originsLimited
- Animal function and withdrawalModerate
- Model safetyLimited
- Human protection and healthspanNot yet determinable
Why can aging muscle become more oxidative while function declines? Cardiolipin and compensation
An oxidative shift can compensate for mitochondrial damage without improving muscle function. A 2026 cardiolipin-depletion study demonstrates that separation: some muscles gain mitochondrial-content…
- Measurements and denominatorsModerate
- Depletion and cellular mechanismModerate
- Animal function and recoveryLimited
- Antioxidants and net effectsLimited
- Human function and healthspanNot yet determinable
Longer lipids with age: a causal change or a shift in lipid composition?
These source tables show relative remodeling within lipid classes in some tissues, which cannot be explained entirely by replacement between classes. But “longer species become relatively favored,”…
- Definitions and samplesModerate
- Age/intervention remodelingModerate
- Animal mechanism/lifespanLimited
- Genetics and membrane physicsLimited
- Human healthspan/applicationsNot yet determinable
Can senolytic CAR T cells selectively remove harmful cells? Target choice and the cost of persistence
Anti-uPAR CAR T cells have produced functional benefits in mice, including improvements in some intestinal barrier, regeneration and inflammation measurements. Treatment early in life can also have…
- Target and measurementModerate
- Mouse functionModerate
- Net value of persistenceNot yet determinable
- Target-related injuryModerate
- Human healthspanNot yet determinable
Why do senescent cells persist: target evasion or failure of immune clearance?
Persistent senescent cells can reflect changes in the target, immune cells and their shared environment. An October 2026 study connects chaperone-mediated autophagy (CMA) to all three: altered…
- CMA and clearance measurementsModerate
- Mechanisms between cellsModerate
- Source tables and cell specificityLimited
- Sustained clearance and feedbackNot yet determinable
- Human applications and lifespanNot yet determinable
Why can STING inhibition help while deleting cGAS worsens aging?
Blocking STING and deleting cGAS are different interventions. The former can reduce some inflammatory signals; the latter removes both a DNA-sensing enzyme and its noncatalytic functions. Mouse and…
- Interventions and multiple functionsModerate
- Mouse functional benefitsModerate
- Recorded lifespan and causalityLimited
- Nuclear functions and inflammatory mediationLimited
- Human applicationsNot yet determinable
Are Longer Telomeres Always Better? Repair, Replication, and Cancer Risk
Longer telomeres may allow some cells to keep dividing, while also allowing cells that have acquired mutations to persist longer. Assessing whether that change is beneficial requires considering…
- Human genetics and familiesModerate
- Mouse survival and safetyLimited
- Human lifespan benefit in healthy peopleNot yet determinable
Can a Softer Environment Restore Regeneration in Aged Cells?
Whether aged cells become active again can depend on their surroundings. For oligodendrocyte progenitor cells involved in myelin repair, the stiffness of a culture material, the matrix they contact…
- Rodent cells and lesion modelsModerate
- Lasting regeneration and human functionNot yet determinable