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Introduction to Fibroblasts

Introduction to Fibroblasts

Rudolph Virchow discovered spindle-shaped cells called fibroblasts in 1858. Inactive fibroblasts, called fibrocytes, become activated by various stimuli, such as growth factors and inflammatory cytokines. Activated fibroblasts play a crucial role in wound healing, inflammation, formation of new blood vessels, and cancer progression. Uncontrolled activation of fibroblasts results in fibrosis, the excess deposition of fibrous tissue, which can lead to scarring and affect normal organs. This...

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Updated: May 17, 2025

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Fibroblast activation protein-targeted chimeric antigen-receptor-modified NK cells alleviate cardiac fibrosis.

Qi Zheng¹, Hao Li¹, Yongliang Jiang²

¹Department of Cardiology, The Second Affiliated Hospital of Kunming Medical University, Kunming, Yunnan 650101, China.

International Immunopharmacology

|May 4, 2025

Summary

This summary is machine-generated.

Engineered CAR natural killer (NK) cells targeting fibroblast activation protein (FAP) effectively reduced cardiac fibrosis in mice. This novel therapy shows promise for treating cardiovascular diseases by eliminating FAP-positive cells and improving heart function.

Keywords:

Cardiac fibrosis Chimeric antigen receptor Fibroblast activation protein Fibroblast-to myofibroblast differentiation Immunotherapy Natural killer cell

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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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Assessing Cardiac Reprogramming using High Content Imaging Analysis

Assessing Cardiac Reprogramming using High Content Imaging Analysis

Published on: October 26, 2020

Area of Science:

Immunotherapy
Cardiovascular Research
Cell Biology

Background:

Cardiac fibrosis (CF) is a key factor in cardiovascular disease progression, involving myofibroblast transdifferentiation.
Fibroblast activation protein (FAP) is a specific marker for activated myofibroblasts.
Chimeric antigen receptor (CAR)-based therapy offers a promising immunotherapy approach.

Purpose of the Study:

To construct CAR natural killer (NK) cells targeting FAP for potential CF therapy.
To evaluate the efficacy and mechanism of FAP-targeted CAR-NK cells in preclinical models of cardiac fibrosis.

Main Methods:

Development of FAP-specific CAR-NK-92 cells.
In vitro assessment of FAP CAR-NK cell cytotoxicity, cytokine secretion, and degranulation against FAP+ cells and cardiac fibroblasts.
In vivo studies using a mouse model of Ang II/PE-induced cardiac injury.

Main Results:

FAP CAR-NK-92 cells specifically recognized and killed FAP+ cells in vitro.
Enhanced cytotoxicity, cytokine secretion, and degranulation of FAP CAR-NK cells compared to parental NK-92 cells.
In vivo administration of FAP CAR-NK cells improved cardiac function and reduced fibrosis, with evidence of increased apoptosis in target cells.

Conclusions:

FAP CAR-NK-92 cells demonstrate specific targeting and potent anti-fibrotic effects in vitro and in vivo.
This CAR-NK cell-based therapy represents a potential therapeutic strategy for cardiac fibrosis patients.