Angiotensin 1‐7 protects against ventilator‐induced diaphragm dysfunction

Yoshihara, Toshinori; Deminice, Rafael; Hyatt, Hayden W.; Özdemir, Merve; Nguyen, Branden L.; Powers, Scott K.

doi:10.1111/cts.13015

Cited by 5 publications

(2 citation statements)

References 43 publications

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“…NPPV фактически считается инструментом выбора в основном у симптоматических пациентов с двусторонним диафрагмальным параличом. Переносимость хорошая, NPPV обеспечивает как клиническое улучшение, так и улучшение показателей газов крови в долгосрочной перспективе [39,40].…”

Section: клиника дисфункции диафрагмыunclassified

Dysfunction of the diaphragm

Uryasev¹,

Glotov²,

Borisovna³

et al. 2022

Medical news of the North Caucasus

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университет им. академика И. п. павлова, Российская Федерация 2 Клиническая больница им. Н. А. Семашко, Рязань, Российская Федерация DYsfuncTion of The Diaphragm uryasev o. m. 1 , glotov s. i. 1 , ponomareva i. B. 1 , almazova e. V. 2 , Zhukova l. a. 1 , alekseeva e. a. 1 1 i. p. pavlov ryazan state medical university, russian federation 2 n. a. semashko clinical hospital, ryazan, russian federationДисфункция диафрагмы относится к редким причинам респираторных нарушений, выраженность которых колеблется от умеренных в случаях ее слабости до выраженных -при параличе диафрагмы. Сложности диагностики дисфункции диафрагмы определяются многообразием этиологических факторов, необычностью клинических проявлений -от субклинических дыхательных расстройств до выраженной дыхательной недостаточности, нередким превалированием общей симптоматики -сонливости, раздражительности, быстрой утомляемости. При параличе диафрагмы возникают выраженные торакоабдоминальные нарушения. Подробно рассмотрены физикальные и инструментальные методы диагностики. В лечении используются как консервативные, так и хирургические методы (пликация диафрагмы). Ключевые слова: дисфункция диафрагмы, одышка, двусторонний паралич диафрагмы, пликация диафрагмыDiaphragm dysfunction refers to the rare causes of respiratory disorders, the severity of which ranges from moderate, in cases of its weakness, to severe -with paralysis of the diaphragm. Difficulties in diagnosing of diaphragm dysfunction are determined by a variety of etiological factors, unusual clinical manifestations -from subclinical respiratory disorders to severe respiratory failure, frequent prevalence of general symptoms -drowsiness, irritability, fatigue. With paralysis of the diaphragm, there are pronounced thoracoabdominal disorders. Physical and instrumental methods of diagnostics are considered in detail. Both conservative and surgical methods (plication of the diaphragm) are used in the treatment.

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Section: клиника дисфункции диафрагмыunclassified

Dysfunction of the diaphragm

Uryasev¹,

Glotov²,

Borisovna³

et al. 2022

Medical news of the North Caucasus

View full text Add to dashboard Cite

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“…In VIDD, the renin-angiotensin system (RAS) causes oxidative stress and induces atrophy via its main peptide angiotensin II. However, RAS also possesses a counterregulatory axis in which the peptide angiotensin (1-7) reduces oxidative stress and proteolysis, thereby protecting against the onset of VIDD [23,24]. Although the results of prior studies clearly show that SIRT1, HSP72, and angiotensin (1-7) are essential for maintaining diaphragm function in VIDD, the intrinsic antiautophagic, antiapoptotic, and antiproteasomal mechanisms for protecting the diaphragm during MV remain unclear.…”

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Identification of the co-differentially expressed hub genes involved in the endogenous protective mechanism against ventilator-induced diaphragm dysfunction

et al. 2022

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Background In intensive care units (ICU), mechanical ventilation (MV) is commonly applied to save patients’ lives. However, ventilator-induced diaphragm dysfunction (VIDD) can complicate treatment by hindering weaning in critically ill patients and worsening outcomes. The goal of this study was to identify potential genes involved in the endogenous protective mechanism against VIDD. Methods Twelve adult male rabbits were assigned to either an MV group or a control group under the same anesthetic conditions. Immunostaining and quantitative morphometry were used to assess diaphragm atrophy, while RNA-seq was used to investigate molecular differences between the groups. Additionally, core module and hub genes were analyzed using WGCNA, and co-differentially expressed hub genes were subsequently discovered by overlapping the differentially expressed genes (DEGs) with the hub genes from WGCNA. The identified genes were validated by western blotting (WB) and quantitative real-time polymerase chain reaction (qRT–PCR). Results After a VIDD model was successfully built, 1276 DEGs were found between the MV and control groups. The turquoise and yellow modules were identified as the core modules, and Trim63, Fbxo32, Uchl1, Tmprss13, and Cst3 were identified as the five co-differentially expressed hub genes. After the two atrophy-related genes (Trim63 and Fbxo32) were excluded, the levels of the remaining three genes/proteins (Uchl1/UCHL1, Tmprss13/TMPRSS13, and Cst3/CST3) were found to be significantly elevated in the MV group (P < 0.05), suggesting the existence of a potential antiproteasomal, antiapoptotic, and antiautophagic mechanism against diaphragm dysfunction. Conclusion The current research helps to reveal a potentially important endogenous protective mechanism that could serve as a novel therapeutic target against VIDD.

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Ventilator‐induced diaphragm dysfunction: phenomenology and mechanism(s) of pathogenesis

Powers

2024

The Journal of Physiology

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Mechanical ventilation (MV) is used to support ventilation and pulmonary gas exchange in patients during critical illness and surgery. Although MV is a life‐saving intervention for patients in respiratory failure, an unintended side‐effect of MV is the rapid development of diaphragmatic atrophy and contractile dysfunction. This MV‐induced diaphragmatic weakness is labelled as ‘ventilator‐induced diaphragm dysfunction’ (VIDD). VIDD is an important clinical problem because diaphragmatic weakness is a risk factor for the failure to wean patients from MV. Indeed, the inability to remove patients from ventilator support results in prolonged hospitalization and increased morbidity and mortality. The pathogenesis of VIDD has been extensively investigated, revealing that increased mitochondrial production of reactive oxygen species within diaphragm muscle fibres promotes a cascade of redox‐regulated signalling events leading to both accelerated proteolysis and depressed protein synthesis. Together, these events promote the rapid development of diaphragmatic atrophy and contractile dysfunction. This review highlights the MV‐induced changes in the structure/function of diaphragm muscle and discusses the cell‐signalling mechanisms responsible for the pathogenesis of VIDD. This report concludes with a discussion of potential therapeutic opportunities to prevent VIDD and suggestions for future research in this exciting field. image

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Angiotensin 1‐7 protects against ventilator‐induced diaphragm dysfunction

Cited by 5 publications

References 43 publications

Dysfunction of the diaphragm

Dysfunction of the diaphragm

Identification of the co-differentially expressed hub genes involved in the endogenous protective mechanism against ventilator-induced diaphragm dysfunction

Ventilator‐induced diaphragm dysfunction: phenomenology and mechanism(s) of pathogenesis

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