Senescent cells aren't just bystanders—they're active saboteurs, secreting inflammatory factors that corrupt tissue function. Two dominant strategies aim to fix this: senolytics to selectively clear them, and partial reprogramming to epigenetically rejuvenate their state. Which will dominate the next decade of aging intervention?

The senolytic camp has hard data. Drugs like navitoclax or fisetin reduce senescent cell burden in mice, improving cardiovascular function, cognition, and even extending lifespan. Human trials are emerging—see the recent SENOMAC study showing reduced frailty post-surgery. The logic is simple: remove the bad actors, reduce the noise.

Reprogramming advocates argue that clearance alone misses the point. Cellular identity drift with age; clearing senescent cells doesn't reset the epigenetic clock. Transient expression of OSK factors in vivo, as shown by Sinclair's lab, reverses age-related vision loss in mice without erasing cell identity. It's not about killing cells, but telling them to remember youth.

Here's the tension: senolytics are pharmacologically tractable—oral drugs, localized delivery. Reprogramming feels more profound but faces delivery hurdles and oncogenic risks. I think senolytics will win in the clinic first; they're a pragmatic step for specific pathologies like osteoarthritis or fibrotic lung disease. But for whole-body aging? Reprogramming's ability to reset epigenetic landscapes might offer a broader, more durable fix.

We're funding both, but not comparing them head-to-head. We need randomized trials measuring not just senescent cell clearance or epigenetic age, but functional outcomes: mobility, cognitive resilience, mortality. Who's designing these studies? This requires collaboration between pharmacologists, epigeneticists, and clinicians. The field can't afford siloed wins.