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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix
Published on: June 14, 2016
The role of periostin in cardiac fibrosis
Bao Qiao1,2,3, Xuehao Liu1,2,3, Bailu Wang4
1Department of Emergency and Chest Pain Center, Qilu Hospital of Shandong University, Jinan, Shandong, 250012, China.
Insights
Cardiac fibrosis, a key factor in heart failure, involves extracellular matrix (ECM) remodeling. This review explores periostin
Area of Science:
- Cardiovascular biology
- Extracellular matrix biology
Background:
- Cardiac fibrosis, characterized by extracellular matrix (ECM) buildup, significantly contributes to heart failure progression.
- Cardiac remodeling, involving altered gene expression in cardiac cells and ECM, is a major cause of morbidity and mortality in heart failure.
- Despite extensive research, the precise mechanisms driving cardiac fibrosis remain incompletely understood.
Purpose of the Study:
- To review the constitutive domain of periostin and its interactions with other ECM proteins.
- To discuss the pathophysiological roles of periostin in cardiac remodeling, including distinct mechanisms.
- To highlight complexities and contentious findings in periostin research.
Main Methods:
- Literature review focusing on periostin's role in cardiac fibrosis and remodeling.
- Analysis of periostin's structure, function, and interactions with ECM components.
- Synthesis of current experimental data and identification of research challenges.
Main Results:
- Periostin, an ECM protein, is crucial for normal cardiac ECM homeostasis and actively regulates cellular reorganization during fibrosis.
- Periostin influences cardiac remodeling through at least two distinct, potentially interconnected pathways.
- Experimental findings regarding periostin's function in cardiac fibrosis present complexities and controversies.
Conclusions:
- Periostin is a significant regulator of cardiac fibrosis and remodeling, impacting ECM structure and cellular behavior.
- Understanding periostin's multifaceted roles is critical for developing therapeutic strategies against heart failure.
- Further research is needed to resolve discrepancies and fully elucidate periostin's contribution to cardiac pathology.
Abstract:
Cardiac fibrosis, which is the buildup of proteins in the connective tissues of the heart, can lead to end-stage extracellular matrix (ECM) remodeling and ultimately heart failure. Cardiac remodeling involves changes in gene expression in cardiac cells and ECM, which significantly leads to the morbidity and mortality in heart failure. However, despite extensive research, the elusive intricacies underlying cardiac fibrosis remain unidentified. Periostin, an extracellular matrix (ECM) protein of the fasciclin superfamily, acts as a scaffold for building complex architectures in the ECM, which improves intermolecular interactions and augments the mechanical properties of connective tissues. Recent research has shown that periostin not only contributes to normal ECM homeostasis in a healthy heart but also serves as a potent inducible regulator of cellular reorganization in cardiac fibrosis. Here, we reviewed the constitutive domain of periostin and its interaction with other ECM proteins. We have also discussed the critical pathophysiological functions of periostin in cardiac remodeling mechanisms, including two distinct yet potentially intertwined mechanisms. Furthermore, we will focus on the intrinsic complexities within periostin research, particularly surrounding the contentious issues observed in experimental findings.
