Collin Y. Ewald

This paper uses a dynamical systems model to explain how late-life lifespan extension in C. elegans occurs through changes in regulatory network stability rather than reversing damage.

This study shows that pharmacologic AMPK activation with MK-8722 extends lifespan in C. elegans and improves metabolic health in aged mice.

This study shows that reducing insulin/IGF-1 signaling in early adulthood extends healthspan and lifespan, but in later life, it accelerates aging and reduces lifespan.

This paper identifies a VHL-1/HIF-1/SQRD-1/COL-88 axis linking extracellular matrix formation with longevity in C. elegans, showing that loss of VHL-1 increases lifespan and alters collagen expression.

The paper measures collagen content in mice tissues and whole bodies, finding collagen constitutes 12% in females and 17% in males of total protein.

The paper identifies hemidesmosome-containing structures that mediate mechanotransduction to regulate ECM homeostasis and promote longevity in C. elegans.

This study shows that condensin I/IDC, not cohesin, is the major genome loop extruder in C. elegans, leading to genome decompaction and loss of TAD structures.

This study shows that longevity interventions in C. elegans temporally scale healthspan rather than compress sickspan, suggesting similar mechanisms may apply in mammals.

The paper uses multi-omics data from mice to identify gene-environment-age interactions and causal molecular networks linked to longevity.

This study shows that late-life targeted degradation of the DAF-2 receptor in C. elegans extends lifespan without growth-related pathologies.

The paper shows that extracellular matrix gene expression can identify cell types and states better than random gene subsets and can match transcription factors in some cases.

The paper defines extracellular matrix phenomes across species by analyzing genotype-to-phenotype relationships and identifies key genes and phenotypes associated with matrisome variations.