Orlando Laitano
University of Florida, FL·Physiology
People who survive sepsis — a body-wide reaction to infection that affects roughly 49 million people a year — often leave the hospital unable to walk well. Up to 75% develop a lasting muscle problem: muscle shrinks, strength drops, and the normal repair process stops working.
- Fields
Physiology
Medicine & Clinical Research
Biology
- Topics
sepsis
skeletal muscle
myopathy
- Grants
- 1 known grant, through Aug 2028
What they work on
- Test whether deleting Nox2, Nox4, or both specifically in muscle fibers — using myoAAV, a virus engineered to enter muscle — protects septic mice from weakness and atrophy during hindlimb disuse, measured by contractile force and muscle mass.
- Determine whether fiber-specific NOX deletion preserves muscle protein synthesis, reduces protein breakdown and inflammatory cell infiltration, and normalizes redox-sensitive protein signatures identified by proteomics in septic, immobilized mice.
- Assess whether reactive oxygen species made by muscle fibers impair satellite cells, the stem cells that repair muscle, by measuring their abundance, proliferation and ability to form new fibers after sepsis.
- Map the transcriptional and epigenetic programs that control satellite cell regenerative potential in septic muscle, and ask whether removing myofiber NOX2 and NOX4 restores them.
More about the research
Long stretches of bed rest during critical illness make it worse, and there is no approved treatment. A central open question is how infection, immobilization and chemical stress inside muscle fibers combine to cause this damage.
Why it matters
Survivors of sepsis frequently face months or years of weakness and frailty, and no therapy currently targets that muscle damage directly. By pinpointing whether specific ROS-producing enzymes inside muscle fibers cause the wasting and block repair, this work could identify drug targets that preserve strength during critical illness and shorten the long recovery that follows an ICU stay.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Ivan Vechetti
University of Nebraska-Lincoln, NE·Physiology
Determine whether MG53, a mitochondria-protecting protein that rises in hibernating ground squirrel muscle, is necessary to lessen skeletal muscle loss during disuse-induced atrophy.
Julia Boster
University of Colorado Denver/Anschutz Medical Campus, CO·Medicine & Clinical Research·Early-career
Measure mitochondrial respiration, reactive oxygen species production and oxidative stress in abdominal muscle from children with chronic cholestasis, using Oroboros O2k respirometry, and relate them to sarcopenia.
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.
The school
University of Florida: 65 labs on PI Pages, $1.3B a year on research, 795 research doctorates a year.
Reach out
A start for your email. Fill in the brackets.