Renin-Angiotensin System Fingerprints of Heart Failure With Reduced Ejection Fraction

Pávó, Noémi; Wurm, Raphael; Goliasch, Georg; Novák, J; Strunk, Guido; Gyöngyösi, Mariann; Poglitsch, Marko; Säemann, Marcus D.; Hülsmann, Martin

doi:10.1016/j.jacc.2016.10.017

Cited by 25 publications

(18 citation statements)

References 4 publications

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“…Commonly evaluated components of the RAAS include plasma renin activity, direct plasma renin levels, plasma or serum aldosterone and AngII concentrations, plasma ACE activity, urine and serum Na + /K + ratios, 24‐hour urinary aldosterone excretion, and the UAldo:C. More recently, liquid chromatography‐mass spectrometry has been used to create a comprehensive renin‐angiotensin system Fingerprint (Attoquant Diagnostics GmbH, Vienna, Austria) from both blood and tissue samples (Figure ) . This comprehensive assessment is beneficial, as looking at only 1 or 2 components of this system might be misleading.…”

Section: Circulating and Tissue Raasmentioning

confidence: 99%

The renin‐angiotensin‐aldosterone system and its suppression

Ames

Atkins

Pitt

2019

Veterinary Internal Medicne

300

264

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Chronic activation of the renin‐angiotensin‐aldosterone system (RAAS) promotes and perpetuates the syndromes of congestive heart failure, systemic hypertension, and chronic kidney disease. Excessive circulating and tissue angiotensin II (AngII) and aldosterone levels lead to a pro‐fibrotic, ‐inflammatory, and ‐hypertrophic milieu that causes remodeling and dysfunction in cardiovascular and renal tissues. Understanding of the role of the RAAS in this abnormal pathologic remodeling has grown over the past few decades and numerous medical therapies aimed at suppressing the RAAS have been developed. Despite this, morbidity from these diseases remains high. Continued investigation into the complexities of the RAAS should help clinicians modulate (suppress or enhance) components of this system and improve quality of life and survival. This review focuses on updates in our understanding of the RAAS and the pathophysiology of AngII and aldosterone excess, reviewing what is known about its suppression in cardiovascular and renal diseases, especially in the cat and dog.

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Section: Circulating and Tissue Raasmentioning

confidence: 99%

The renin‐angiotensin‐aldosterone system and its suppression

Ames

Atkins

Pitt

2019

Veterinary Internal Medicne

300

264

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“…The abovementioned released cardiac cytokines and other inflammatory mediators not only affect the heart but also different organs as outlined below. Furthermore, several neurohormonal mechanisms that become activated in HF to try and sustain cardiac output in the face of decompensating function [145, 146] also affect inflammation in different organs.…”

Section: Heart Failure Causes Inflammationmentioning

confidence: 99%

Inflammation – Cause or Consequence of Heart Failure or Both?

Linthout

Tschöpe

2017

Curr Heart Fail Rep

347

288

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Purpose of ReviewWith the intention to summarize the currently available evidence on the pathophysiological relevance of inflammation in heart failure, this review addresses the question whether inflammation is a cause or consequence of heart failure, or both.Recent FindingsThis review discusses the diversity (sterile, para-inflammation, chronic inflammation) and sources of inflammation and gives an overview of how inflammation (local versus systemic) can trigger heart failure. On the other hand, the review is outlined how heart failure-associated wall stress and signals released by stressed, malfunctioning, or dead cells (DAMPs: e.g., mitochondrial DNA, ATP, S100A8, matricellular proteins) induce cardiac sterile inflammation and how heart failure provokes inflammation in various peripheral tissues in a direct (inflammatory) and indirect (hemodynamic) manner. The crosstalk between the heart and peripheral organs (bone marrow, spleen, gut, adipose tissue) is outlined and the importance of neurohormonal mechanisms including the renin angiotensin aldosteron system and the ß-adrenergic nervous system in inflammation and heart failure is discussed.SummaryInflammation and heart failure are strongly interconnected and mutually reinforce each other. This indicates the difficulty to counteract inflammation and heart failure once this chronic vicious circle has started and points out the need to control the inflammatory process at an early stage avoiding chronic inflammation and heart failure. The diversity of inflammation further addresses the need for a tailored characterization of inflammation enabling differentiation of inflammation and subsequent target-specific strategies. It is expected that the characterization of the systemic and/or cardiac immune profile will be part of precision medicine in the future of cardiology.

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“…Further, Acuna et al reported that the genetic deletion or antagonist A779 of Mas deteriorated muscular architecture and increased fibrosis and TGF-β signalling with diminished muscle strength in dystrophic MDX mice, suggesting that endogenous Mas in skeletal muscle is relevant for protection against pathological muscle remodelling [72]. However, given the alternative pathway of Ang 1-7 production by neprilysin [30][31][32], it remains undetermined whether the proposed role of endogenous Mas in muscle remodelling is completely linked to the catalytic activity of ACE2. Studies using ACE2-function-deficient animals may be helpful in drawing conclusions about this subject.…”

Section: Muscle Remodellingmentioning

confidence: 99%

“…To date, no study has been reported on the function of alamandine in skeletal muscle. While ACE2 is a major determinant in regulating the tissue level of Ang 1-7, neprilysin, a type-II integral membrane protein that cleaves angiotensin I to Ang 1-7 also participates in the regulation of the tissue and plasma levels of Ang 1-7 [30][31][32]. Neprilysin also cleaves Ang 1-7 to small peptides as well as ACE [33,34], and angiotensin 1-2, the proteolytic product of neprylisin, has been shown to be relevant in pancreatic insulin secretion [35].…”

Section: Introductionmentioning

confidence: 99%

ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19

2020

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Angiotensin converting enzyme-2 (ACE2) is a multifunctional transmembrane protein recently recognised as the entry receptor of the virus causing COVID-19. In the renin–angiotensin system (RAS), ACE2 cleaves angiotensin II (Ang II) into angiotensin 1-7 (Ang 1-7), which is considered to exert cellular responses to counteract the activation of the RAS primarily through a receptor, Mas, in multiple organs including skeletal muscle. Previous studies have provided abundant evidence suggesting that Ang 1-7 modulates multiple signalling pathways leading to protection from pathological muscle remodelling and muscle insulin resistance. In contrast, there is relatively little evidence to support the protective role of ACE2 in skeletal muscle. The potential contribution of endogenous ACE2 to the regulation of Ang 1-7-mediated protection of these muscle pathologies is discussed in this review. Recent studies have suggested that ACE2 protects against ageing-associated muscle wasting (sarcopenia) through its function to modulate molecules outside of the RAS. Thus, the potential association of sarcopenia with ACE2 and the associated molecules outside of RAS is also presented herein. Further, we introduce the transcriptional regulation of muscle ACE2 by drugs or exercise, and briefly discuss the potential role of ACE2 in the development of COVID-19.

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Renin-Angiotensin System Fingerprints of Heart Failure With Reduced Ejection Fraction

Cited by 25 publications

References 4 publications

The renin‐angiotensin‐aldosterone system and its suppression

The renin‐angiotensin‐aldosterone system and its suppression

Inflammation – Cause or Consequence of Heart Failure or Both?

ACE2, angiotensin 1-7 and skeletal muscle: review in the era of COVID-19

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