“This work establishes a new framework for understanding how inter-organelle crosstalk contributes to aging and highlights peroxisome degradation as a potential target for interventions aimed at preserving mitochondrial function and extending lifespan.”

BUFFALO, NY — July 21, 2026 — A new research paper was published in Volume 18 of Aging on July 6, 2026, titled “Inhibition of peroxisomal protein PRX-11 promotes longevity in Caenorhabditis elegans via enhancements to mitochondria.”

The study was authored by Yash Flora, Dhriti Shastri, Kathryn R. DeLeo, and K. Adam Bohnert from the Department of Biological Sciences, Louisiana State University.

Aging is accompanied by the gradual decline of many cellular structures that help maintain healthy tissues and organs. Among these are peroxisomes, which play essential roles in breaking down toxic molecules and metabolizing lipids, and mitochondria, which generate most of the cell’s energy. Although these organelles work closely together, little has been known about how changes in one influence the aging of the other. This new study reveals that preserving peroxisomes helps maintain healthier mitochondria and extends lifespan in the nematode Caenorhabditis elegans, providing new insight into how communication between cellular organelles influences aging.

In this study, the researchers investigated the function of PRX-11, a peroxisomal protein involved in peroxisome division. Previous work from the group showed that reducing PRX-11 activity prevents the age-related degradation of peroxisomes through a process known as pexophagy and increases lifespan. The new study explored why preserving peroxisomes produces these beneficial effects and found that maintaining peroxisomes also preserves mitochondrial health during aging.

The researchers found that animals with reduced PRX-11 activity retained long, interconnected mitochondrial networks that resembled those seen in young adults, whereas normal aging was associated with progressive mitochondrial fragmentation. These preserved mitochondria also accumulated less calcium, generated lower levels of oxidative stress, maintained higher ATP-to-ADP ratios, and were associated with improved locomotor function in older animals. Together, these findings indicate that preventing age-related peroxisome loss supports multiple aspects of mitochondrial function during aging.

The study also identified several key regulators required for these protective effects. The improvements in mitochondrial health depended on FZO-1/Mitofusin, UNC-43 protein kinase, and the longevity-associated transcription factor DAF-16/FOXO. When any of these factors was disrupted, inhibition of PRX-11 no longer preserved mitochondrial structure or extended lifespan, demonstrating that mitochondrial integrity is essential for the longevity benefits associated with maintaining peroxisomes.

Importantly, the relationship between peroxisomes and mitochondria proved to be bidirectional. Animals with genetically impaired mitochondrial function experienced accelerated peroxisome degradation early in adulthood, suggesting that dysfunction in either organelle can negatively influence the other. This reciprocal interaction supports the concept that aging results from coordinated changes across multiple cellular systems rather than deterioration of individual organelles in isolation.

Beyond lifespan, the researchers observed broader improvements in physiological health. Animals with reduced PRX-11 activity showed enhanced energy metabolism, larger lipid reserves, lower oxidative stress, and better preservation of movement during aging. These findings suggest that maintaining peroxisome homeostasis promotes healthier aging by supporting cellular metabolism and preserving mitochondrial performance.

“Our data support a model in which peroxisomes and mitochondria track together with age and interdependently influence animal lifespan.”

According to the authors, preserving peroxisome function may represent a previously underappreciated strategy for protecting mitochondrial health during aging. They propose that targeting age-related peroxisome degradation could help maintain cellular function and promote healthier aging by strengthening communication between these two essential organelles.

Overall, this study demonstrates that preventing the age-associated loss of peroxisomes helps preserve mitochondrial structure and function while extending lifespan in C. elegans. By revealing a close functional partnership between peroxisomes and mitochondria during aging, the findings establish a new framework for understanding how communication between cellular organelles contributes to longevity and identifies peroxisome homeostasis as a promising area for future aging research.

Paper DOI: https://doi.org/10.18632/aging.206395                      

Corresponding author: K. Adam Bohnert – [email protected]        

Keywords: cellular aging, lifespan, pexophagy, mitochondrial tubulation, inter-organelle crosstalk

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