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Davis Englund, PhD

@DavisEnglund

Assistant Professor @UABHeersink. Aging, cellular senescence, and skeletal muscle biology.
Birmingham, AL sites.uab.edu/englundlab/ Joined June 2011
535 Following 977 Followers 2.3K Posts

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Davis Englund, PhD @DavisEnglund
Really nice write-up by Katie Cottingham in @UABNews highlighting our lab’s work!

@UABDeptMed @UABHeersink
UAB @UABNews May 20
UAB researchers review how senescent “zombie” cells contribute to skeletal muscle weakness with aging and disease, outlining emerging therapies such as senolytics and senomorphics that could help preserve muscle health and extend health span. go.uab.edu/42e78hN
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Davis Englund, PhD @DavisEnglund
Really enjoyed this conversation on skeletal muscle, aging, and cellular senescence. Thanks to the Healthspan team for the opportunity to discuss our work and the broader importance of maintaining muscle health across the lifespan!
Healthspan Verified account @healthspanmed Jun 16
Muscle mass peaks in your 30s, then declines 3–8% per decade.

By age 80, you've lost roughly 30–50% of the muscle you had at your physiological peak.

In this week's Beyond Healthspan podcast, we talk to Dr. Davis Englund (@DavisEnglund) about what drives that decline at the cellular level—and why senescent cells accumulating in muscle are a primary mechanism.

Senescent cells don't just occupy space. They actively block muscle regeneration through inflammatory signaling that disrupts satellite cell function—the stem cells responsible for muscle repair.

When Englund's group measured blood-based senescence markers in older adults, baseline senescence predicted training response. Higher senescent cell burden meant poorer adaptation to exercise.

The implication: muscle decline during aging isn't just atrophy from disuse. It's an accumulation of damaged cells that sabotage the repair machinery.

Englund explains:

- Why senolytics help muscle repair in old mice but harm it in young ones
- Which cell types in muscle become senescent (fibers vs. satellite cells)
- How mTOR hyperactivity during aging drives sarcopenia instead of growth
- Why exercise itself appears to have senolytic effects
- The difference between clearing senescent cells and suppressing their inflammatory output
- Why tissue-specific senolytics are the next therapeutic frontier
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Davis Englund, PhD @DavisEnglund
Thanks, Matt! Already looking forward to next year.
Myself and the rest of the @UABExerciseMed had a great time at the Tornado Alley Muscle Meeting last week. Outstanding talks from @ThalackerMercer @DavisEnglund and their trainees. Kudos to @KevinMurachPhD @DavisEnglund and the other organizers for putting on a great meeting.
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