Why the study?
Diaphragm weakness impairs quality of life, exercise capacity, and survival in patients with chronic heart failure and reduced left ventricular ejection fraction, but the underlying cellular mechanisms in humans remain poorly resolved.
Patients with severe heart failure demonstrate a distinct diaphragm myopathy characterized by fiber atrophy, oxidative stress, and mitochondrial dysfunction, independent of disuse or other confounding factors.
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Identifies cellular targets in CHF diaphragm myopathy; leaves open whether these mechanisms are modifiable or prognostic.
Mangner et al. (2021) studied this question.
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