Intercellular communication lessons in heart failure

Bang, Claudia; Antoniades, Charalambos; Antonopoulos, Alexios S; Eriksson, Ulf; Franssen, Constantijn; Hamdani, Nazha; Lehmann, Lorenz; Moessinger, Christine; Mongillo, Marco; Muhl, Lars; Speer, Thimoteus; Thum, Thomas

doi:10.1002/ejhf.399

Cited by 50 publications

(40 citation statements)

References 137 publications

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“…Those cells are not only active in producing collagens but they also act as inflammatory support cells via their capacity to express chemokines, to release factors inducing adhesion molecules on endothelial cells, and via their ability to stimulate monocytes to express gelatinases facilitating degradation of the basolateral membrane and subsequent infiltration of immune cells in the heart [23, 24] and their capacity to modulate the MΦ M1/M2 balance [72]. Furthermore, activated fibroblasts promote cardiomyocyte hypertrophy and dysfunction via the release of pro-fibrotic factors, such as TGF-β1, Ang II, and fibroblast growth factor [73, 74]. …”

Section: Inflammationmentioning

confidence: 99%

Inflammation – Cause or Consequence of Heart Failure or Both?

Linthout

Tschöpe

2017

Curr Heart Fail Rep

346

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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Section: Inflammationmentioning

confidence: 99%

Inflammation – Cause or Consequence of Heart Failure or Both?

Linthout

Tschöpe

2017

Curr Heart Fail Rep

346

288

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“…Indeed, a thorough characterization of vascular and microvascular function in experimental HFpEF is warranted and will pave the way for preclinical testing. Unveiling the complete pathophysiological scenario, however, will require an in‐depth understanding of the cellular disturbances and complex interplay between endothelium, cardiomyocytes, and fibroblasts as well as the high‐order interactions with other tissues (see supplementary material online, Figure S1). Dysfunctional interactions between cardiac cell‐types have been proposed, but while various intercellular communication disturbances have been well documented in related experimental models and cell culture experiments, few were documented in HFpEF .…”

Section: Gaps In Evidence What Do We Need For a Systems Biology Apprmentioning

confidence: 99%

An integrative translational approach to study heart failure with preserved ejection fraction: a position paper from the Working Group on Myocardial Function of the European Society of Cardiology

Lourenço

Leite‐Moreira

Balligand

et al. 2017

European J of Heart Fail

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As heart failure with preserved ejection fraction (HFpEF) rises to epidemic proportions, major steps in patient management and therapeutic development are badly needed. With the current position paper we seek to update our view on HFpEF as a highly complex systemic syndrome, from risk factors and mechanisms to long-term clinical manifestations. We will revise recent advances in animal model development, experimental set-ups and basic and translational science approaches to HFpEF research, highlighting their drawbacks and advantages. Directions are provided for proper model selection as well as for integrative functional evaluation from the in vivo setting to in vitro cell function testing. Additionally, we address new research challenges that require integration of higher-order inter-organ and inter-cell communication to achieve a full systems biology perspective of HFpEF.

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“…These fibroblasts are responsible for the homeostatic maintenance of the ECM and interact with cardiomyocytes through paracrine signaling [10,11]. Cardiac fibroblasts also drive the process of ECM remodeling.…”

Section: Introductionmentioning

confidence: 99%

Altered protein levels in the isolated extracellular matrix of failing human hearts with dilated cardiomyopathy

DeAguero

McKown

Zhang

et al. 2017

Cardiovascular Pathology

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Dilated cardiomyopathy (DCM) is associated with extensive pathological cardiac remodeling and involves numerous changes in the protein expression profile of the extracellular matrix of the heart. We obtained seven human, end-stage, failing hearts with DCM (DCM-failing) and nine human, nonfailing donor hearts and compared their extracellular matrix protein profiles. We first showed that the DCM-failing hearts had indeed undergone extensive remodeling of the left ventricle myocardium relative to nonfailing hearts. We then isolated the extracellular matrix from a subset of these hearts and performed a proteomic analysis on the isolated matrices. We found that the levels of 26 structural proteins were altered in the DCM-failing isolated cardiac extracellular matrix compared to nonfailing isolated cardiac extracellular matrix. Overall, most of the extracellular matrix proteins showed reduced levels in the DCM-failing hearts, while all of the contractile proteins showed increased levels. There was a mixture of increased and decreased levels of cytoskeletal and nuclear transport proteins. Using immunoprobing, we verified that collagen IV (α2 and α6 isoforms), zyxin, and myomesin protein levels were reduced in the DCM-failing hearts. We expect that these data will add to the understanding of the pathology associated with heart failure with DCM.

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Intercellular communication lessons in heart failure

Cited by 50 publications

References 137 publications

Inflammation – Cause or Consequence of Heart Failure or Both?

Inflammation – Cause or Consequence of Heart Failure or Both?

An integrative translational approach to study heart failure with preserved ejection fraction: a position paper from the Working Group on Myocardial Function of the European Society of Cardiology

Altered protein levels in the isolated extracellular matrix of failing human hearts with dilated cardiomyopathy

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