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Decoding menopause-induced tissue fibrosis using pan-tissue network inference.

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Summary

This summary is machine-generated.

Menopause causes fibrosis across organs by altering immune cell signaling. Estrogen-responsive macrophages act as key hubs, interacting with myofibroblasts, revealing conserved and tissue-specific mechanisms of menopausal dysfunction.

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Mechanistic Insight into the Development of TNBS-Mediated Intestinal Fibrosis and Evaluating the Inhibitory Effects of Rapamycin

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Published on: September 12, 2019

Area of Science:

Immunology
Systems Biology
Fibrosis Research

Background:

Menopause induces fibrotic remodeling and organ dysfunction.
Mechanisms of menopause-driven fibrosis are not fully understood.
Immune cells play a critical role in inflammation and fibrosis.

Purpose of the Study:

To investigate conserved and tissue-specific mechanisms of menopause-driven fibrosis.
To map intercellular signaling shifts in immune cells during menopause.
To identify potential therapeutic targets for menopausal dysfunction.

Main Methods:

Network inference framework applied to single-cell RNA-sequencing data.
Analysis of liver, lung, pancreas, and skeletal muscle from ovariectomized and control mice.
Reconstruction of cell-cell interaction networks focusing on immune cells.

Main Results:

Menopause reshapes intercellular signaling across multiple tissues.
Estrogen-responsive macrophages act as conserved signaling hubs interacting with myofibroblasts.
Tissue-specific immune cell signaling patterns were identified, including NK cells in muscle.

Conclusions:

A systems-level network approach reveals conserved immune-stromal modules in menopausal fibrosis.
Estrogen-responsive macrophages are central to menopause-associated fibrosis.
Targeting these conserved modules may prevent menopause-related organ dysfunction.