The DOI matches its Crossref record; 175 of the 175 references it cites were found in a registry or an index.
Inflammation – Cause or Consequence of Heart Failure or Both?
Open accessAbstract
PURPOSE OF REVIEW: With 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 FINDINGS: This 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. Inflammation 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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2016 ESC Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure
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Self-citationSterile inflammation: sensing and reacting to damage
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Cited by
Groenewegen, A., Rutten, F. H., Mosterd, A., & Hoes, A. W. (2020) · European Journal of Heart Failure · doi:10.1002/ejhf.1858 · Cited by 2,043
Wang, S., Song, R., Wang, Z., Jing, Z., Wang, S., & Ma, J. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.01298 · Cited by 1,450
The Clinical Significance of Interleukin-6 in Heart Failure: Results from the BIOSTAT-CHF Study
Markousis-Mavrogenis, G., Tromp, J., Ouwerkerk, W., Devalaraja, M., Anker, S. D., Cleland, J. G., Dickstein, K., Filippatos, G. S., van der Harst, P., Lang, C. C., et al. (2019) · European Journal of Heart Failure · doi:10.1002/ejhf.1482 · Cited by 294
Byrne, N. J., Matsumura, N., Maayah, Z. H., Ferdaoussi, M., Takahara, S., Darwesh, A. M., Levasseur, J. L., Jahng, J. W. S., Vos, D., Parajuli, N., et al. (2020) · Circulation: Heart Failure · doi:10.1161/circheartfailure.119.006277 · Cited by 257
Mitochondrial DNA as an inflammatory mediator in cardiovascular diseases
Nakayama, H., & Otsu, K. (2018) · Biochemical Journal · doi:10.1042/bcj20170714 · Cited by 160
Metadata
- Authors
- Van Linthout, S., & Tschöpe, C.
- Venue
- Current Heart Failure Reports
- Published
- 2017-06-30
- Volume
- 14
- Issue
- 4
- Pages
- 251-265
- ISSN
- 1546-9530 (ISSN-L)
- 1546-9549
- OpenAlex
- W2730107310
- Cited by
- 465
- References
- 175
- FWCI
- 27.36
- Type
- journal article
- Language
- en
- Open access
- hybrid
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