ArticleBiogerontology2026
Evaluating pharmacological targeting of actin regulatory pathways during aging in C. elegans.
Article in Biogerontology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Actin is a highly conserved cytoskeletal protein that regulates numerous cellular processes essential for tissue homeostasis and healthy aging. Although genetic studies have established important roles for actin and actin-binding proteins in longevity, pharmacological approaches offer complementary advantages for manipulating conserved cytoskeletal pathways across model systems. Here, we systematically evaluated the effects of small-molecule modulators targeting distinct actin regulatory pathways on lifespan, locomotor function, and tissue-specific actin organization in Caenorhabditis elegans. Animals were treated with compounds targeting the Arp2/3 complex (CK666), tropomyosin-dependent actin regulation (TR100), formins (SMIFH2), cofilin regulation (SZ-3), or actin stabilization (phalloidin). Among the compounds tested, only CK666 consistently produced a dose-dependent reduction in lifespan and exacerbated age-associated muscle actin disorganization, identifying Arp2/3-mediated actin branching as a critical regulator of cytoskeletal integrity during aging. CK666 also transiently disrupted hypodermal actin organization early in adulthood. In contrast, SMIFH2, TR100, phalloidin, and SZ-3 produced little or no detectable disruption of muscle actin organization, despite previous genetic studies demonstrating roles for several of these pathways in aging. Comparison with prior RNAi studies suggests that pharmacological perturbation can reproduce some aspects of actin dysfunction but may be limited by compound stability, drug delivery, or inefficient targeting of proteins in C. elegans. Together, these findings establish a framework for evaluating pharmacological modulation of actin during aging, identify CK666-mediated Arp2/3 inhibition as the most robust pharmacological perturbation under the conditions tested, and highlight important considerations for translating genetic discoveries into pharmacological strategies to target cytoskeletal function during aging.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.