Inflammatory mediators drive adverse right ventricular remodeling and dysfunction and serve as potential biomarkers
Frontiers in Physiology, ISSN: 1664-042X, Vol: 9, Issue: MAY, Page: 609
2018
- 48Citations
- 50Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
Citation Benchmarking is provided by Scopus and SciVal and is different from the metrics context provided by PlumX Metrics.
Metrics Details
- Citations48
- Citation Indexes48
- 48
- Captures50
- Readers50
- 50
Review Description
Adverse right ventricular (RV) remodeling leads to ventricular dysfunction and failure that represents an important determinant of outcome in patients with pulmonary hypertension (PH). Recent evidence indicates that inflammatory activation contributes to the pathogenesis of adverse RV remodeling and dysfunction. It has been shown that accumulation of inflammatory cells such as macrophages and mast cells in the right ventricle is associated with maladaptive RV remodeling. In addition, inhibition of inflammation in animal models of RV failure ameliorated RV structural and functional impairment. Furthermore, a number of circulating inflammatory mediators have been demonstrated to be associated with RV performance. This work reviews the role of inflammation in RV remodeling and dysfunction and discusses anti-inflammatory strategies that may attenuate adverse structural alterations while promoting improvement of RV function.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85047432405&origin=inward; http://dx.doi.org/10.3389/fphys.2018.00609; http://www.ncbi.nlm.nih.gov/pubmed/29875701; https://www.frontiersin.org/article/10.3389/fphys.2018.00609/full; https://dx.doi.org/10.3389/fphys.2018.00609; https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2018.00609/full
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