Compartmental analysis of steady-state diaphragm Ca2+ kinetics in chronic congestive heart failure

Domínguez, Jesús Fernández; Howell, S.

doi:10.1016/s0143-4160(02)00208-7

Cited by 12 publications

(17 citation statements)

References 49 publications

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“…Results from previous studies indicate that calpains are able to cleave both titin and nebulin [34,35]. Indeed, increased calpain activities have been reported in diaphragm of HF rats [36]. Titin proteolysis by calpains leaves the cleavage product T2 [35].…”

Section: Causes Of Protein Loss In Hfmentioning

confidence: 95%

Heart failure decreases passive tension generation of rat diaphragm fibers

Hees

Ottenheijm

Granzier

et al. 2010

International Journal of Cardiology

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Section: Causes Of Protein Loss In Hfmentioning

confidence: 95%

Heart failure decreases passive tension generation of rat diaphragm fibers

Hees

Ottenheijm

Granzier

et al. 2010

International Journal of Cardiology

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“…Based on findings reported in limb muscles of old [93] and CHF animals [94,95] and patients [96], it is reasonable to speculate that aging or CHF impairs diaphragm calcium release. In diaphragm preparations, CHF slows calcium reuptake, which appears to be caused by decreases in sarcoplasmic reticulum calcium-ATPase expression [97–99]. Thus, abnormalities in E-C coupling may contribute to diaphragm dysfunction in CHF and aging.…”

Section: Intrinsic Diaphragm Muscle Abnormalitiesmentioning

confidence: 99%

“…Pigs with CHF induced by supraventricular tachycardia have 20–40% lower cross-sectional area of type I, IIa, and IIB fibers [13]. In rats, CHF induced by myocardial infarction results in a 15% to 25% decrease in fiber cross-sectional area in some studies [11,117,97], but unchanged fiber cross-sectional area has been reported by our group [112] and others [75,111]. Similarly, there was no diaphragm atrophy in rats during late stages of CHF due to aortic stenosis [86].…”

Section: Intrinsic Diaphragm Muscle Abnormalitiesmentioning

confidence: 99%

“…These antecedent processes are performed at least partially by calpains [181], which are activated by calcium. CHF dysregulates calcium homeostasis in the diaphragm such that intracellular calcium concentration is elevated and calpain activity is increased two-fold [97]. Calpain activation, which causes diaphragm weakness in sepsis and mechanical ventilation [182,183], is a plausible process that mediates diaphragm weakness in CHF, but a cause-and-effect relationship has not been established.…”

Section: Cellular Mediators Of Diaphragm Abnormalities In Chfmentioning

confidence: 99%

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Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology

Kelley

Ferreira

2016

Heart Fail Rev

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Inspiratory function is essential for alveolar ventilation and expulsive behaviors that promote airway clearance (e.g., coughing and sneezing). Current evidence demonstrates that inspiratory dysfunction occurs during healthy aging and is accentuated by chronic heart failure (CHF). This inspiratory dysfunction contributes to key aspects of CHF and aging cardiovascular and pulmonary pathophysiology including: i) impaired airway clearance and predisposition to pneumonia; ii) inability to sustain ventilation during physical activity; iii) shallow breathing pattern that limits alveolar ventilation and gas exchange; and iv) sympathetic activation that causes cardiac arrhythmias and tissue vasoconstriction. The diaphragm is the primary inspiratory muscle, hence, its neuromuscular integrity is a main determinant of the adequacy of inspiratory function. Mechanistic work within animal and cellular models has revealed specific factors that may be responsible for diaphragm neuromuscular abnormalities in CHF and aging. These include phrenic nerve and neuromuscular junction alterations as well as intrinsic myocyte abnormalities, such as changes in the quantity and quality of contractile proteins, accelerated fiber atrophy, and shifts in fiber type distribution. CHF, aging, or CHF in the presence of aging disturbs the dynamics of circulating factors (e.g., cytokines and angiotensin II) and cell signaling involving sphingolipids, reactive oxygen species, and proteolytic pathways, thus leading to the previously listed abnormalities. Exercise-based rehabilitation combined with pharmacological therapies targeting the pathways reviewed herein hold promise to treat diaphragm abnormalities and inspiratory muscle dysfunction in CHF and aging.

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“…Na insuficiência cardíaca, o prejuízo nas proteínas relacionadas ao transporte intracelular de Ca 2+ , supracitado, poderia ter como consequência uma exacerbação das concentrações desse íon capaz de ativar essas proteases. 35 Já o sistema ubiquitina-proteossoma tem como princípio a degradação de peptídeos, muitas vezes provenientes da clivagem pelas calpaínas, "etiquetados" com ubiquitinas. Essa ubiquitinação é principalmente regulada por enzimas chamadas E3 ligases, que catalisam a transferência de ubiquitinas ativadas e conjugadas em um complexo de poliubiquitinas para a proteína-alvo, que é então reconhecida pelo proteossoma 26S (organela do citoplasma com pH ácido) e degradada em pequenos peptídeos.…”

Section: Alterações Molecularesunclassified

Relevância e tratamento das lesões características da insuficiência cardíaca na musculatura esquelética

Júnior

2009

Medicina (Ribeirão Preto)

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Pacientes com insuficiência cardíaca, a via final das doenças cardiovasculares e a primeira causa de internação em idosos no Brasil, apresentam deterioração do tecido muscular esquelético. Além disso, as lesões na musculatura têm relação direta com a qualidade de vida e a autonomia dos pacientes, por meio do nível de tolerância aos esforços físicos, além de constituírem um preditor independente de mortalidade na síndrome. Ao longo da presente revisão de literatura serão discutidos em relação à insuficiência cardíaca: seu conceito e um breve histórico; a importância da musculatura esquelética; as anormalidades funcionais, estruturais, bioquímicos e moleculares que acometem esse tecido; as potenciais causas dessas alterações (hiperatividade simpática, redução na ingestão alimentar, espécies reativas de oxigênio, citocinas pró-inflamatórias e diminuição do nível de atividade física e do fluxo sanguíneo); e os efeitos da principal terapia direcionada para combater essa disfunção, o treinamento físico aeróbio de intensidade moderada. Reconhecida a importância do tecido muscular esquelético na síndrome, essa é uma área da investigação científica com muitos temas ainda não estudados, como o efeito de terapias farmacológicas utilizadas pelos pacientes, de exercícios físicos aeróbios de maior intensidade e intervalados, de exercícios físicos de força, de intervenções nutricionais e de terapias celulares e gênicas. No futuro, os resultados desses estudos que serão desenvolvidos certamente contribuirão para uma menor degeneração da musculatura esquelética na doença, o que, consequentemente, vai melhorar a ualidade de vida, a autonomia e o prognóstico dos pacientes.

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Compartmental analysis of steady-state diaphragm Ca2+ kinetics in chronic congestive heart failure

Cited by 12 publications

References 49 publications

Heart failure decreases passive tension generation of rat diaphragm fibers

Heart failure decreases passive tension generation of rat diaphragm fibers

Diaphragm abnormalities in heart failure and aging: mechanisms and integration of cardiovascular and respiratory pathophysiology

Relevância e tratamento das lesões características da insuficiência cardíaca na musculatura esquelética

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