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Scanning Electron Microscopy of Macerated Tissue to Visualize the Extracellular Matrix

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Mechanical communication in fibrosis progression.

Yi Long¹, Yudi Niu², Kaini Liang²

¹Department of Biomedical Engineering, School of Medicine, Tsinghua-Peking Center for Life Sciences, Tsinghua University, Beijing, 100084, China; Joint Graduate Program of Peking-Tsinghua-National Institute of Biological Science, Tsinghua University, Beijing, 100084, China.

Trends in Cell Biology

|November 23, 2021

Summary

This summary is machine-generated.

Fibrotic microenvironments involve complex mechanical signals between cells and their surroundings. This study explores cellular responses to these cues and engineering models for developing new fibrosis treatments.

Keywords:

fibrosis mechanical crosstalk mechano-based therapeutics mechanotransduction

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Area of Science:

Biomedical Engineering
Mechanobiology
Fibrosis Research

Background:

Fibrotic microenvironments are characterized by mechanical forces that drive disease progression.
Cells interact with the extracellular matrix (ECM) and hemodynamic forces, but understanding this interplay is challenging.
Abnormal hemodynamics and ECM remodeling activate intracellular mechanotransduction pathways in fibrotic diseases.

Purpose of the Study:

To explore mechanical communication in cell-ECM, cell-hemodynamics, and cell-ECM-cell crosstalk during fibrosis.
To provide an overview of engineering systems for modeling fibrosis.
To identify and predict mechano-based therapeutic targets for fibrosis.

Main Methods:

Review of current literature on mechanotransduction in fibrotic diseases.
Analysis of cell-ECM and cell-hemodynamics interactions.
Overview of in vitro and in silico engineering systems for disease modeling.

Main Results:

Mechanical cues from ECM remodeling and abnormal hemodynamics are central to fibrosis.
Cell-ECM, cell-hemodynamics, and cell-ECM-cell (paratensile signaling) crosstalk are key mechanisms.
Engineering systems offer promising avenues for studying fibrosis and identifying therapeutic targets.

Conclusions:

Understanding mechanical communication is crucial for addressing fibrosis progression.
In vitro and in silico models can advance the identification of mechano-therapeutic targets.
Targeting mechanical pathways presents a novel strategy for treating fibrotic diseases.