Nonlinear H₂O₂ scavenging by peroxiredoxins drives acquired stress resistance and replicative lifespan hormesis.

Biological and pharmacokinetic studies indicate that the anti-tubercular drug, delamanid, could be repurposed for the treatment of visceral leishmaniasis.

Multi-omics reveals that Alkb homolog 7 (ALKBH7), α mitochondrial alpha-ketoglutarate dioxygenase of unclear function, regulates glyoxal metabolism, which may explain its role in necrosis and heart attack.

In-built competing effects are present at different levels in signaling networks, starting from basic biochemical building blocks to the network level, and mathematical and computational analysis reveals when they give rise to biphasic responses and what the consequences are.

The transcriptomic profiles of the constituent monotherapies of synergistic drug pairs tend to be correlated and result in novel gene expression in the combinations.

Genetic analysis reveals NADPH oxidase generated reactive oxygen species as signals to re-establish cellular homeostasis during aging via activating a transcriptional response.

As worms age reduced glutathione together with increased ferrous iron increases frailty and leads to ferroptosis, which is amenable to therapeutic intervention.

Human cells adapt to chronic mild stresses, such as slightly elevated temperature, by getting larger in a process that couples increased translation to increased cell size in an Hsp90-dependent manner.

Cardiomyocyte Nox4 is a crucial physiological mediator of Nrf2 activation during acute exercise, triggering an adaptive response that preserves redox balance, mitochondrial and cardiac function to support normal physical exercise.

Aging is a process characterized by gradual metabolome remodeling, deceleration of the remodeling in late life and under conditions that extend lifespan, and a mortality-associated pattern of cumulative damage.