Davis Englund
University of Alabama at Birmingham, AL·Physiology·Early-career
Muscles shrink and weaken with age, a syndrome called sarcopenia that costs older adults independence and drives heavy health care use. There are no effective drugs, partly because the underlying cell biology is unsettled.
- Fields
Physiology
Biology
Medicine & Clinical Research
- Topics
cellular senescence
sarcopenia
skeletal muscle
- Grants
- 1 known grant, through Aug 2027
What they work on
- Define the core features of muscle fiber senescence by overexpressing p21, a cell-cycle-halting protein, in muscle fibers of living mice and combining validated senescence markers with transcriptome-wide analysis to find candidate therapeutic targets.
- Test whether senescent cell burden directly impairs muscle by comparing gain-of-function and loss-of-function p21 mouse models on measures of muscle size, strength and overall muscle health.
- Determine why only some nuclei inside a multi-nucleated muscle fiber become senescent, using myonuclear isolation and multiomic profiling to compare senescent and non-senescent myonuclei.
- Assess the feasibility of targeting senescent cells to restore muscle size and function in sarcopenic mice, generating the preliminary data needed to evaluate senolytic approaches.
More about the research
One candidate culprit is cellular senescence: cells that stop dividing but do not die, instead lingering and releasing inflammatory signals. Senescent cells pile up with age and at sites of disease, and in mice removing them improves health in several tissues. Muscle poses a puzzle, though, because mature muscle fibers are long, multi-nucleated cells that have already stopped dividing, so whether they can become senescent at all is an open question.
Why it matters
Sarcopenia erodes quality of life in older adults and has no approved treatment. By testing whether senescent muscle fibers actively cause muscle loss and weakness, this work could establish senescent cells, and the p21 pathway that drives them, as a druggable target for preventing or treating age-related muscle decline, and would clarify how an aging mechanism operates in a tissue made of cells that no longer divide.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Sabrina Spencer
University of Colorado Boulder, CO·Biochemistry
Test whether p16, a protein that naturally blocks the kinases CDK4 and CDK6, controls the rebound of CDK2 activity seen in single cells hours after CDK2 inhibition, using time-lapse microscopy of living cells.
Toren Finkel
University of Pittsburgh, PA·Biology
Build a high-resolution map of senescent cells, cells that stop dividing permanently, in human lung and heart, using single-cell RNA and ATAC sequencing, proteomics and spatial transcriptomics.
Yanjiao Zhou
University of Connecticut, CT·Microbiology & Immunology
Test whether senescent cells reshape the gut microbiome and its metabolites by transplanting or genetically clearing senescent cells in older male and female mice, using the p21-Cre mouse model.
The school
University of Alabama at Birmingham: 45 labs on PI Pages, $866M a year on research, 166 research doctorates a year.
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