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Related Experiment Video

Updated: May 12, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

Published on: August 3, 2018

IHG-1 must be localised to mitochondria to decrease Smad7 expression and amplify TGF-β1-induced fibrotic responses.

James B Corcoran¹, Sarah McCarthy, Brenda Griffin

¹School of Medicine and Medical Sciences, University College Dublin, Belfield, Dublin, Ireland.

Biochimica Et Biophysica Acta

|April 10, 2013

Summary

This summary is machine-generated.

Mitochondrial protein IHG-1 amplifies kidney fibrosis signaling by suppressing Smad7. A non-mitochondrial IHG-1 mutant inhibits fibrosis, highlighting mitochondria

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Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

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Published on: September 14, 2021

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Last Updated: May 12, 2026

Molecular Analysis of Endothelial-mesenchymal Transition Induced by Transforming Growth Factor-β Signaling

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Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Visualization and Quantification of TGFβ/BMP/SMAD Signaling under Different Fluid Shear Stress Conditions using Proximity-Ligation-Assay

Published on: September 14, 2021

Area of Science:

Cell Biology
Molecular Biology
Renal Pathophysiology

Background:

Transforming growth factor-beta 1 (TGF-β1) is a key driver of organ fibrosis.
Induced in high glucose-1 (IHG-1) is a mitochondrial protein linked to kidney disease.
IHG-1 amplifies TGF-β1 responses and regulates mitochondrial biogenesis.

Purpose of the Study:

To investigate the role of mitochondrial localization of IHG-1 in TGF-β1 signaling.
To determine how IHG-1 affects the expression of the TGF-β1 inhibitor Smad7.
To assess the fibrotic signaling effects of a non-mitochondrial IHG-1 mutant.

Main Methods:

Expression analysis of IHG-1 and Smad7 in renal cells.
Utilized a non-mitochondrial deletion mutant of IHG-1 (Δmts-IHG-1).
Assessed TGF-β1-induced fibrotic gene expression (CCN2, fibronectin, jagged-1).
Investigated Smad7's role in mediating Δmts-IHG-1's effects via knockdown experiments.

Main Results:

Mitochondrial localization of IHG-1 is crucial for amplifying TGF-β1 signaling.
IHG-1 expression correlates with reduced Smad7 protein levels.
Expression of Δmts-IHG-1 repressed TGF-β1-induced fibrotic signaling and increased Smad7.
Δmts-IHG-1's inhibitory effect on TGF-β1 signaling depends on Smad7 expression.

Conclusions:

Mitochondria play a significant role in modulating TGF-β1 signal transduction.
IHG-1 is a critical mediator in the mitochondrial regulation of TGF-β1 signaling.
Targeting IHG-1's mitochondrial function may offer a therapeutic strategy for kidney fibrosis.