Literature DB >> 26739214

The crossroads of inflammation, fibrosis, and arrhythmia following myocardial infarction.

Samantha D Francis Stuart1, Nicole M De Jesus1, Merry L Lindsey2, Crystal M Ripplinger3.   

Abstract

Optimal healing of damaged tissue following myocardial infarction (MI) requires a coordinated cellular response that can be divided into three phases: inflammatory, proliferative/reparative, and maturation. The inflammatory phase, characterized by rapid influx of cytokines, chemokines, and immune cells, is critical to the removal of damaged tissue. The onset of the proliferative/reparative phase is marked by increased proliferation of myofibroblasts and secretion of collagen to replace dead tissue. Lastly, crosslinking of collagen fibers and apoptosis of immune cells marks the maturation phase. Excessive inflammation or fibrosis has been linked to increased incidence of arrhythmia and other MI-related pathologies. This review describes the roles of inflammation and fibrosis in arrhythmogenesis and prospective therapies for anti-arrhythmic treatment.
Copyright © 2015 Elsevier Ltd. All rights reserved.

Entities:  

Keywords:  Arrhythmia; Fibrosis; Inflammation; Myocardial infarction

Mesh：

Substances：

Year:  2015        PMID： 26739214      PMCID： PMC4764395          DOI： 10.1016/j.yjmcc.2015.12.024

Source DB:  PubMed          Journal:  J Mol Cell Cardiol        ISSN： 0022-2828            Impact factor:   5.000


  89 in total

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4.  Targeting cardiac fibrosis: a new frontier in antiarrhythmic therapy?

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5.  CCR5 signaling suppresses inflammation and reduces adverse remodeling of the infarcted heart, mediating recruitment of regulatory T cells.

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Authors:  Lisa Chilton; Wayne R Giles; Godfrey L Smith
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Review 8.  Macrophage roles following myocardial infarction.

Authors:  Jessica M Lambert; Elizabeth F Lopez; Merry L Lindsey
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Review 1.  Matrix metalloproteinases as input and output signals for post-myocardial infarction remodeling.

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Journal:  J Mol Cell Cardiol       Date:  2015-12-23       Impact factor: 5.000

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Review 4.  Heart Disease and Relaxin: New Actions for an Old Hormone.

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Journal:  Expert Rev Proteomics       Date:  2018-01-09       Impact factor: 3.940

6.  Dynamic Chromatin Targeting of BRD4 Stimulates Cardiac Fibroblast Activation.

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7.  Astragaloside IV enhances cardioprotection of remote ischemic conditioning after acute myocardial infarction in rats.

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8.  Spermidine-enhanced autophagic flux improves cardiac dysfunction following myocardial infarction by targeting the AMPK/mTOR signalling pathway.

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Review 9.  Role of the microRNA-29 family in myocardial fibrosis.

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Review 10.  Use of Interleukin-1 Blockers in Pericardial and Cardiovascular Diseases.

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