Annals of vascular surgery · 2026
Skeletal Muscle Mass and Quality in Peripheral Artery Disease: New Insights into Clinical Management and Therapeutic Optimization.
СтатьяОбзорНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
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Nishibe Toshiya, Kano Masaki, Fukuda Shoji, Koizumi Jun, Nishibe Masayasu, Dardik Alan
Аннотация
BACKGROUND: Peripheral artery disease (PAD) induces chronic limb ischemia that affects downstream skeletal muscle and leads to ischemic myopathy. Chronic ischemia results in mitochondrial dysfunction, oxidative stress, fiber-type shift, proteolysis, and anabolic resistance, contributing to reduced endurance and persistent weakness despite revascularization.
METHODS: This narrative review provides a clinically oriented synthesis of PAD-related muscle pathology, pragmatic approaches to assessing muscle mass and quality, and current strategies to preserve or restore muscle health.
RESULTS: Chronic ischemia impairs mitochondrial biogenesis, increases reactive oxygen species, activates ubiquitin-proteasome and autophagy-lysosome pathways, and suppresses IGF-1/Akt/mTOR signaling, resulting in muscle atrophy and qualitative degeneration. Endothelial dysfunction and pro-inflammatory macrophage polarization further limit regeneration. Assessment begins with the ankle-brachial index and functional screening, followed by segmental bioimpedance or bedside ultrasound, with selective computed tomography or magnetic resonance imaging. Although exercise improves walking performance, endurance-only programs may inadequately preserve limb muscle, whereas resistance-inclusive training better maintains muscle mass and quality. Revascularization restores perfusion and mitigates ischemia, thereby preparing a physiological environment that supports, but does not by itself ensure, rehabilitation-driven improvements in skeletal muscle and functional recovery. Conventional PAD drugs reduce vascular risk but show limited direct muscle effects; mechanism-based therapies remain investigational.
CONCLUSION: Recognizing skeletal muscle as a therapeutic target supports an integrated management approach combining revascularization, resistance-inclusive exercise, nutritional optimization, and emerging muscle-directed therapies to improve mobility and clinical outcomes.
METHODS: This narrative review provides a clinically oriented synthesis of PAD-related muscle pathology, pragmatic approaches to assessing muscle mass and quality, and current strategies to preserve or restore muscle health.
RESULTS: Chronic ischemia impairs mitochondrial biogenesis, increases reactive oxygen species, activates ubiquitin-proteasome and autophagy-lysosome pathways, and suppresses IGF-1/Akt/mTOR signaling, resulting in muscle atrophy and qualitative degeneration. Endothelial dysfunction and pro-inflammatory macrophage polarization further limit regeneration. Assessment begins with the ankle-brachial index and functional screening, followed by segmental bioimpedance or bedside ultrasound, with selective computed tomography or magnetic resonance imaging. Although exercise improves walking performance, endurance-only programs may inadequately preserve limb muscle, whereas resistance-inclusive training better maintains muscle mass and quality. Revascularization restores perfusion and mitigates ischemia, thereby preparing a physiological environment that supports, but does not by itself ensure, rehabilitation-driven improvements in skeletal muscle and functional recovery. Conventional PAD drugs reduce vascular risk but show limited direct muscle effects; mechanism-based therapies remain investigational.
CONCLUSION: Recognizing skeletal muscle as a therapeutic target supports an integrated management approach combining revascularization, resistance-inclusive exercise, nutritional optimization, and emerging muscle-directed therapies to improve mobility and clinical outcomes.