Eben Estell
University of New England, ME·Physiology·Early-career
Physical activity makes bones stronger, but the chemical conversation between working muscle and the skeleton is only partly mapped. One candidate messenger is irisin, a small signaling protein that muscle releases during exercise.
- Fields
Physiology
Biology
Pharmacology
- Topics
irisin
Fndc5
osteoclast
- Grants
- 1 known grant, through Jan 2028
What they work on
- Map the signaling pathway irisin triggers inside osteoclasts, the bone-dissolving cells, by confirming candidate receptors including integrin αVβ5 and tracking the intracellular steps that lead to differentiation and resorption in culture.
- Test whether muscle-derived irisin is required for bone to respond to exercise, using a newly developed conditional Fndc5 mouse allele deleted specifically in skeletal muscle.
- Determine whether irisin reaches osteoclasts indirectly through osteocytes, the load-sensing cells embedded in bone, by measuring osteocyte-derived signals such as sclerostin and RANKL after irisin exposure.
- Examine whether irisin signaling alters how osteocytes sense mechanical cues, testing the interplay between loading-induced responses and irisin during skeletal adaptation.
More about the research
Knowing exactly what irisin tells bone cells to do would explain how the skeleton adapts to loading, and could reveal a natural pathway worth borrowing for treating bone-weakening disease.
Why it matters
Degenerative bone diseases such as the bone loss that follows estrogen decline are a growing burden as populations age. Clarifying how an exercise-released muscle signal instructs bone-dissolving and bone-building cells could identify drug targets that work with the body's own loading-response pathways, rather than against them, and may help explain why exercise protects the skeleton.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sarah Dallas
University of Missouri-Kansas City, MO·Physiology
Determine how osteoblast movement, differentiation and fate are tied to collagen assembly and mineralization, using live-cell and intravital imaging of mice with GFP-tagged type I collagen and bone-lineage fluorescent reporters.
Beata Lecka-Czernik
University of Toledo, OH·Physiology
Determine how fuel choice and aging change osteocyte function and whether these effects depend on PPARG, using aged C57BL/6 and osteocyte-specific PPARG knockout mice, bone organ cultures and MLO-Y4 osteocyte-like cells with PPARG knocked down, with transcriptomics and quantitative proteomics.
Hongshuai Li
University of Iowa, IA·Physiology
Identify which cells in dystrophic skeletal muscle produce the bone-regulating myokine FGF21 and the molecular signals that switch it on, using DMD mouse models.
The school
University of New England: 2 labs on PI Pages, $8M a year on research, 71 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.