Bumsoo Ahn
Wake Forest University, NC·Physiology·Early-career
As people age, muscles shrink and weaken, a condition called sarcopenia. This loss erodes mobility and independence in older adults.
- Fields
Physiology
Medicine & Clinical Research
Pharmacology
- Topics
sarcopenia
muscle aging
cancer cachexia
- Grants
- 2 known grants, through Jan 2031
What they work on
- Test whether unacylated ghrelin (UnAG) combined with endurance exercise boosts mitochondrial energy production and lowers oxidative stress in skeletal muscle of older mice, compared with either treatment alone.
- Determine whether UnAG, endurance exercise, or both preserve motor neurons and reduce inflammation in the spinal cord and at the neuromuscular junction, where nerves connect to muscle, in aging mice.
- Measure effects of UnAG plus endurance exercise on muscle mass, contractile force and protein quality in older mice, using transcriptomics to identify the genes and pathways each intervention changes.
- Determine whether UnAG prevents age-related neurogenic muscle atrophy by altering rates of muscle protein synthesis and degradation, measured as protein turnover in living mice.
- Test whether UnAG prevents age-related muscle weakness by improving calcium handling and the calcium sensitivity of contractile filaments in muscle fibers.
- Test whether UnAG prevents the rapid wasting and loss of contractile function caused by cancer cachexia in mice.
More about the research
Exercise is the best known remedy, but older bodies respond to training less strongly than young ones. Muscle wasting also strikes people with cancer, a condition called cachexia, and no drug currently slows it. Both projects test whether unacylated ghrelin (UnAG), a form of a natural hormone whose blood levels fall with age, can protect muscle. One tests UnAG on its own in aging and cancer; the other tests whether UnAG boosts the benefits of exercise.
Why it matters
Older adults with sarcopenia and people with cancer cachexia lose muscle and strength, often losing mobility and independence, and no drug currently treats this. UnAG and its mimetics have good safety records in humans and show no link to cancer cell growth. If the mouse results hold, they could support clinical trials, and pairing UnAG with exercise could become the first combination approach that helps aging muscle respond to training.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Osvaldo Delbono
Wake Forest University, NC·Neuroscience
Define how brainstem A5 sympathetic neurons projecting to hindlimb muscles affect motor denervation, neuromuscular junction signaling and muscle mass and strength with aging, using optogenetics and retrograde labeling in living mice.
Christopher Sundberg
University of Wisconsin-Madison, WI·Physiology
Measure how the protein content of slow and fast muscle fibers changes as they shrink with age in older males and females, using single-fiber proteomics and 3D fiber imaging on the same fibers.
Kandy Velazquez
University of South Carolina-Columbia, SC·Physiology
Determine how TGFβ2, a signaling protein, starts fibrosis (scar-like tissue buildup) and activates M2 macrophages in the skeletal muscle of cancer cachectic mice.
The school
Wake Forest University: 27 labs on PI Pages, $345M a year on research, 54 research doctorates a year.
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