AgingOct 22, 2026

From Overactive Processes to Widespread Boosts: Rethinking How Aging Can Be Reversed

Longevity & Aging Weekly Brief ↗PubMed ↗DOI ↗

Updated Oct 23, 2026

Abstract

The Gompertz law indicates an exponential acceleration of late-life mortality, suggesting an active component in aging.

Aging may be influenced by a systemic hyperfunction of intercellular signaling, which amplifies the effects of cellular damage.
Rapid organism-level rejuvenation can occur through systemic interventions, challenging the view that aging results solely from gradual repair.
Primary lesions are viewed as damage loads, while systemic communication determines the gain in the aging process.
Therapeutic strategies may need to shift focus in different life stages, with early interventions targeting prevention and late-life treatments requiring systemic resets.
Rejuvenation can be understood as a change in regulatory states rather than just the repair of cellular lesions.

Simplified

Aging is often modeled, and interventions prioritized, as the near-linear accumulation of cell-intrinsic lesions; yet the exponential acceleration of late-life mortality under the Gompertz law points to an active, program-like component shaping the trajectory. Furthermore, systemic interventions - including therapeutic plasma exchange and extracellular-vesicle-based therapies - together with the transient embryonic rejuvenation phase, can induce rapid, broadly coordinated organism-level rejuvenation on timescales difficult to attribute to gradual repair alone. Here, we propose an integrative-first load-gain framework in which primary lesions provide the damage load, while the systemic communication architecture sets the gain: a systemic hyperfunction of intercellular signaling that converts slow cellular inputs into self-amplifying late-life acceleration. This architecture provides a mechanistic basis for both the embryonic biological-age reset and Gompertzian late-life acceleration by positioning organism-level coupling as a central gain-setting layer governing aging trajectories. It further implies regime-dependent therapeutic leverage: cell-autonomous approaches are most effective as early-life prevention and may slow progression in midlife, but durable late-life reversal requires systemic signaling reset that suppresses amplification and restores buffering capacity. By treating rejuvenation as a shift in the organism's regulatory state rather than local lesion repair, the framework positions partial reprogramming and other cell-autonomous strategies as complementary to systemic recalibration and most effective within a rejuvenated systemic milieu.

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From Overactive Processes to Widespread Boosts: Rethinking How Aging Can Be Reversed

Abstract

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