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Related Experiment Video

Updated: May 31, 2026

Calcification of Vascular Smooth Muscle Cells and Imaging of Aortic Calcification and Inflammation

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Published on: May 31, 2016

Calcium influx drives m6A-dependent RUNX1T1 splicing to promote adipogenic commitment.

Weiqian Jiang¹, Mingjie Sun¹, Keyu Wei¹

¹Department of Orthopedics, the Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.

|May 29, 2026

Summary

This summary is machine-generated.

Altered calcium signaling drives fibro-adipogenic progenitor (FAP) fat infiltration in sarcopenia. Restoring RUNX1T1-L isoform corrects defects, unlike FTO inhibition, revealing calcium

Keywords:

CP: Metabolism CP: Molecular biology CaM FAPs FTO-m6A-RUNX1T1 axis adipogenesis calcium channel blockers calcium signaling

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Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Mechanism of Regulation of Adipocyte Numbers in Adult Organisms Through Differentiation and Apoptosis Homeostasis

Published on: June 3, 2016

Area of Science:

Cell Biology
Molecular Biology
Metabolic Diseases

Background:

Intermuscular fat infiltration by fibro-adipogenic progenitors (FAPs) drives sarcopenia progression.
This fat infiltration is linked to altered calcium signaling pathways.
Understanding this link is crucial for developing effective sarcopenia therapies.

Purpose of the Study:

To investigate the role of calcium signaling dyshomeostasis in FAP-driven adipogenesis.
To identify molecular mechanisms linking calcium signaling to FAP fate determination.
To explore therapeutic strategies targeting this pathway for sarcopenia.

Main Methods:

Utilized FAP-based adipogenesis models.
Performed structural and biochemical analyses.
Conducted transcriptomic profiling and in vivo drug exposure studies.

Main Results:

Calcium influx dyshomeostasis promotes adipogenic commitment via calmodulin remodeling, KCNQ1-CaM-FTO complex dissociation, FTO nuclear translocation, and m6A-dependent RUNX1T1 alternative splicing.
This cascade reduces the lipogenesis-restrictive RUNX1T1-L isoform, reinforcing the C/EBPα-PPARγ feedback loop.
RUNX1T1-L restoration ameliorated adipogenesis, stemness, and senescence defects more effectively than FTO inhibition; amlodipine treatment led to increased mesenteric fat and liver steatosis in mice.

Conclusions:

Calcium signaling is intricately linked to RNA processing-dependent cell fate control in FAPs.
RUNX1T1-L isoform restoration presents a promising therapeutic avenue for sarcopenia.
Broad calcium channel blockade may have unintended metabolic consequences, such as increased fat accumulation and liver steatosis.