Atrial fibrosis underlying atrial fibrillation (Review)

Li, Chang Yi; Zhang, Jingrui; Hu, Wan; Li, Song Nan

doi:10.3892/ijmm.2020.4842

Cited by 56 publications

(52 citation statements)

References 141 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…A majority of the known proliferative, profibrotic and proinflammatory effects of angiotensin II (Ang II, AT II) occur through interaction with the type 1 angiotensin receptor (AT 1 -R). Ang II binding to AT 1 -R stimulates the mitogen-activated protein kinase (MAPK) and thus regulates the transcription of the target genes: MMP, plasminogen activator inhibitor 1 (PAI-1), CTGF, TGF-β [ 10 ] ( Figure 1 ). The effects of activation of that pathway include fibroblast proliferation and hypertrophy, which lead to increased numbers of fibroblasts and myofibroblasts producing ECM proteins.…”

Section: Neurohormonal Mechanismsmentioning

confidence: 99%

“…The above mentioned risk factors contribute to structural changes within the atrium, including its dilatation and fibrotic processes [ 8 ]. Moreover, a cardiac rhythm disturbance is a result of atrial remodelling, including structural and electrical transformation, and favouring making the changes permanent [ 9 , 10 ]. Making the changes in atrial structure and electric function permanent, leading to more frequent recurrences of arrhythmia episodes is more pronounced in older patients [ 11 , 12 ].…”

Section: Introductionmentioning

confidence: 99%

“…Adaptive changes of the left atrium (LA) myocytes in response to the effects of external factors are necessary for maintaining homeostasis and they lead to left atrial remodelling [ 10 ]. Left atrial fibrosis, which contributes to the development and progression of atrial fibrillation, is regarded as an important marker of the risk of adverse effects in AF patients [ 16 ].…”

Section: Introductionmentioning

confidence: 99%

“…In this review paper we focused on the mechanisms of fibrosis and structural transformation of the heart atria, including neurohormonal disorders mainly of the renin-angiotensin-aldosterone system (RAAS) and activity of the profibrotic pathways initiated by the transforming growth factor beta (TGF-β), platelet-derived growth factor (PDGF) and also connective tissue growth factor (CTGF). It is worth to mention that RAAS plays the key role in the development of the syndrome of tissue responses at both electrical and structural levels [ 10 ]. We also discuss the disturbances of extracellular matrix homeostasis and the role of matrix metalloproteins and their inhibitors in fibrotic processes.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation

Sygitowicz

Maciejak-Jastrzębska

Sitkiewicz

2021

JCM

View full text Add to dashboard Cite

The cellular and molecular mechanism involved in the pathogenesis of atrial fibrosis are highly complex. We have reviewed the literature that covers the effectors, signal transduction and physiopathogenesis concerning extracellular matrix (ECM) dysregulation and atrial fibrosis in atrial fibrillation (AF). At the molecular level: angiotensin II, transforming growth factor-β1, inflammation, and oxidative stress are particularly important for ECM dysregulation and atrial fibrotic remodelling in AF. We conclude that the Ang-II-MAPK and TGF-β1-Smad signalling pathways play a major, central role in regulating atrial fibrotic remodelling in AF. The above signalling pathways induce the expression of genes encoding profibrotic molecules (MMP, CTGF, TGF-β1). An important mechanism is also the generation of reactive oxygen species. This pathway induced by the interaction of Ang II with the AT2R receptor and the activation of NADPH oxidase. Additionally, the interplay between cardiac MMPs and their endogenous tissue inhibitors of MMPs, is thought to be critical in atrial ECM metabolism and fibrosis. We also review recent evidence about the role of changes in the miRNAs expression in AF pathophysiology and their potential as therapeutic targets. Furthermore, keeping the balance between miRNA molecules exerting anti-/profibrotic effects is of key importance for the control of atrial fibrosis in AF.

show abstract

Section: Neurohormonal Mechanismsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation

Sygitowicz

Maciejak-Jastrzębska

Sitkiewicz

2021

JCM

View full text Add to dashboard Cite

show abstract

“…Therefore, FGF-23 can also be used as a marker of myocardial fibrosis. Besides, TGF-β1, as an essential fibrosis mediator, promotes the synthesis of collagen fibers through typical Smad-dependent and non-classical Smad-independent pathways and can also be used as an indirect marker of myocardial fibrosis ( 9 , 10 ).…”

Section: Introductionmentioning

confidence: 99%

Changes in Intestinal Flora Structure and Metabolites Are Associated With Myocardial Fibrosis in Patients With Persistent Atrial Fibrillation

Liu

et al. 2021

Front. Nutr.

View full text Add to dashboard Cite

Background: The occurrence of atrial fibrillation is often accompanied by myocardial fibrosis. An increasing number of studies have shown that intestinal flora is involved in the occurrence and development of a variety of cardiovascular diseases. This study explores the relationship between changes in the structure and function of intestinal flora and the progression of myocardial fibrosis in patients with persistent atrial fibrillation.Methods: Serum and stool samples were collected from 10 healthy people and 10 patients with persistent atrial fibrillation (PeAF), and statistical analyses were performed on the subjects' clinical baseline conditions. ELISA was used to measure the levels of carboxy-terminal telopeptide of type I collagen (CTX-I), propeptide of type I procollagen (PICP), procollagen III N-terminal propeptide (PIIINP), fibroblast growth factor-23 (FGF-23), and transforming growth factor-beta 1 (TGF-β1) in serum. Through 16S rRNA sequencing technology, the structural composition of the intestinal flora was detected and analyzed. In addition, metabolomics data were analyzed to determine the differences in the metabolites produced by the intestinal flora of the subjects.Results: By comparing the baseline data of the subjects, it was found that compared with those of the control group, the levels of creatinine (CRE) and serum uric acid (SUA) in the serum of PeAF patients were significantly increased. In addition, we found that the levels of CTX-I, PICP, PIIINP, and TGF-β1 in the serum of PeAF patients were significantly higher than those of the control group subjects. Although the control and PeAF groups exhibited no significant differences in the α diversity index, there were significant differences in the β diversity indexes (Bray-Curtis, weighted UniFrac and Anosim). At the phylum, family and species levels, the community structure and composition of the intestinal flora of the control group and those of the PeAF group showed significant differences. In addition, the compositions of the intestinal metabolites in the two different groups of people were significantly different. They were correlated considerably with PIIINP and specific communities in the intestinal flora.Conclusion: Pathologically, PeAF patients may have a higher risk of myocardial fibrosis. Systematically, abnormal changes in the structure and composition of the intestinal flora in PeAF patients may lead to differences in intestinal metabolites, which are involved in the process of myocardial fibrosis through metabolite pathways.

show abstract

Keeping the Heartbeat Off-Target in Cancer Therapy

Starobin

Kwaku

2022

JAMA Oncol

View full text Add to dashboard Cite

Atrial fibrosis underlying atrial fibrillation (Review)

Cited by 56 publications

References 141 publications

A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation

A Review of the Molecular Mechanisms Underlying Cardiac Fibrosis and Atrial Fibrillation

Changes in Intestinal Flora Structure and Metabolites Are Associated With Myocardial Fibrosis in Patients With Persistent Atrial Fibrillation

Keeping the Heartbeat Off-Target in Cancer Therapy

Contact Info

Product

Resources

About