Sex-Specific Aspects of Skeletal Muscle Metabolism in the Clinical Context of Intensive Care Unit-Acquired Weakness

Engelhardt, Lilian Jo; Grunow, Julius J.; Wollersheim, Tobias; Carbon, Niklas M.; Balzer, Felix; Spranger, Joachim; Weber‐Carstens, Steffen

doi:10.3390/jcm11030846

Cited by 9 publications

(5 citation statements)

References 27 publications

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“…2002; Engelhardt et al. 2022). These findings underscore the need to examine how sepsis affects mitophagy and mitochondrial dysfunction in skeletal muscles of female mice.…”

Section: Discussionmentioning

confidence: 99%

“…Some studies report higher sepsis-related mortality in men, whereas others report higher mortality in women (Failla & Connelly 2017;Kondo et al 2021;Sakr et al 2013;Schroder et al 1998). Furthermore, sex-based variations have been observed in the extent of metabolic derangement, muscle fibre atrophy and the duration of skeletal muscle weakness in sepsis patients (De Jonghe et al 2002;Engelhardt et al 2022). These findings underscore the need to examine how sepsis affects mitophagy and mitochondrial dysfunction in skeletal muscles of female mice.…”

Section: Impact Of Sepsis On Muscle Mitophagymentioning

confidence: 99%

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Lack of compensatory mitophagy in skeletal muscles during sepsis

Sedraoui,

Leduc‐Gaudet,

Mayaki

et al. 2024

The Journal of Physiology

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Skeletal muscle dysfunction is a major problem in critically ill patients suffering from sepsis. This condition is associated with mitochondrial dysfunction and increased autophagy in skeletal muscles. Autophagy is a proteolytic mechanism involved in eliminating dysfunctional cellular components, including mitochondria. The latter process, referred to as mitophagy, is essential for maintaining mitochondrial quality and skeletal muscle health. Recently, a fluorescent reporter system called mito‐QC (i.e. mitochondrial quality control) was developed to specifically quantify mitophagy levels. In the present study, we used mito‐QC transgenic mice and confocal microscopy to morphologically monitor mitophagy levels during sepsis. To induce sepsis, Mito‐QC mice received Escherichia coli lipopolysaccharide (10 mg kg–1 i.p.) or phosphate‐buffered saline and skeletal muscles (hindlimb and diaphragm) were excised 48 h later. In control groups, there was a negative correlation between the basal mitophagy level and overall muscle mitochondrial content. Sepsis increased general autophagy in both limb muscles and diaphragm but had no effect on mitophagy levels. Sepsis was associated with a downregulation of certain mitophagy receptors (Fundc1, Bcl2L13, Fkbp8 and Phbb2). The present study suggests that general autophagy and mitophagy can be dissociated from one another, and that the characteristic accumulation of damaged mitochondria in skeletal muscles under the condition of sepsis may reflect a failure of adequate compensatory mitophagy. imageKey points There was a negative correlation between the basal level of skeletal muscle mitophagy and the mitochondrial content of individual muscles. Mitophagy levels in limb muscles and the diaphragm were unaffected by lipopolysaccharide (LPS)‐induced sepsis. With the exception of BNIP3 in sepsis, LPS administration induced either no change or a downregulation of mitophagy receptors in skeletal muscles.

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“…2002; Engelhardt et al. 2022). These findings underscore the need to examine how sepsis affects mitophagy and mitochondrial dysfunction in skeletal muscles of female mice.…”

Section: Discussionmentioning

confidence: 99%

Section: Impact Of Sepsis On Muscle Mitophagymentioning

confidence: 99%

Lack of compensatory mitophagy in skeletal muscles during sepsis

Sedraoui,

Leduc‐Gaudet,

Mayaki

et al. 2024

The Journal of Physiology

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“…Not only in chronic disease, but also in acute conditions of critical illness, insulin resistance has been linked to impaired mitochondrial biogenesis [ 180 ]. The phenomenon of insulin resistance was highlighted as a metabolic hallmark feature in critical illness myopathy and ICUAW [ 90 , 181 , 182 ]. Furthermore, overall gastrointestinal function may be impaired especially in critically ill patients with neuromuscular alterations [ 183 ].…”

Section: Structural and Functional Impairments Of Mitochondria In Icu...mentioning

confidence: 99%

Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review

Klawitter

Ehler

Bajorat

et al. 2023

IJMS

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Mitochondria are key structures providing most of the energy needed to maintain homeostasis. They are the main source of adenosine triphosphate (ATP), participate in glucose, lipid and amino acid metabolism, store calcium and are integral components in various intracellular signaling cascades. However, due to their crucial role in cellular integrity, mitochondrial damage and dysregulation in the context of critical illness can severely impair organ function, leading to energetic crisis and organ failure. Skeletal muscle tissue is rich in mitochondria and, therefore, particularly vulnerable to mitochondrial dysfunction. Intensive care unit-acquired weakness (ICUAW) and critical illness myopathy (CIM) are phenomena of generalized weakness and atrophying skeletal muscle wasting, including preferential myosin breakdown in critical illness, which has also been linked to mitochondrial failure. Hence, imbalanced mitochondrial dynamics, dysregulation of the respiratory chain complexes, alterations in gene expression, disturbed signal transduction as well as impaired nutrient utilization have been proposed as underlying mechanisms. This narrative review aims to highlight the current known molecular mechanisms immanent in mitochondrial dysfunction of patients suffering from ICUAW and CIM, as well as to discuss possible implications for muscle phenotype, function and therapeutic approaches.

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“…Due to an Editorial Office error during processing, a number of male and female symbols were incorrectly shown in the pdf version of the manuscript [ 1 ]. In particular, all male and female symbols were shown as male symbols.…”

Section: Text Correctionmentioning

confidence: 99%