# REAC RGN-AR treatment modulates adipogenic differentiation in adipose tissue-derived stem cells

**Authors:** Sara Cruciani, Salvatore Rinaldi, Vania Fontani, Margherita Maioli

PMC · DOI: 10.1038/s41598-026-35204-2 · 2026-01-08

## TL;DR

This study shows that a new treatment called REAC TO RGN-AR can prevent fat cell formation in stem cells while promoting healthier cell types.

## Contribution

The novel use of REAC TO RGN-AR to modulate ADSC differentiation by altering bioelectrical activity is presented.

## Key findings

- REAC TO RGN-AR increased stemness gene expression (Oct-4, Sox2, Nanog) and reduced adipogenic markers (PPAR-γ, LPL, ACOT2).
- Treated cells shifted toward beige adipocytes with increased TMEM26 and reduced ASC-1 expression.

## Abstract

Adipose tissue-derived stem cells (ADSCs) possess multipotent differentiation potential and significant immunomodulatory properties, making them valuable in regenerative medicine. However, their adipogenic differentiation can lead to triglyceride accumulation, chronic inflammation, and metabolic dysfunction. This study evaluated the effects of Radio Electric Asymmetric Conveyer (REAC) technology tissue optimization regenerative adipogenesis reprogramming (TO RGN-AR) on ADSC differentiation, focusing on its ability to preserve stemness, suppress adipogenesis, and promote beneficial phenotypes. REAC TO RGN-AR treatment significantly increased the expression of stemness-related genes (Oct-4, Sox2, and Nanog) while downregulating the expression of adipogenic markers (PPAR-γ, LPL, and ACOT2). Additionally, REAC TO RGN-AR treated cells presented a phenotypic shift toward beige adipocytes, characterized by increased TMEM26 expression and reduced ASC-1 expression. These findings underscore the novelty of using REAC TO RGN-AR to modulate cellular endogenous bioelectrical activity, presenting a noninvasive and operator-independent approach to enhance ADSC-based therapies. This work highlights the potential of this treatment to address metabolic disorders and chronic inflammation while advancing regenerative medicine.

## Linked entities

- **Genes:** POU5F1 (POU class 5 homeobox 1) [NCBI Gene 5460], SOX2 (SRY-box transcription factor 2) [NCBI Gene 6657], NANOG (Nanog homeobox) [NCBI Gene 79923], PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468], LPL (lipoprotein lipase) [NCBI Gene 4023], ACOT2 (acyl-CoA thioesterase 2) [NCBI Gene 10965], TMEM26 (transmembrane protein 26) [NCBI Gene 219623], RPL3 (ribosomal protein L3) [NCBI Gene 6122]

## Full-text entities

- **Genes:** LPL (lipoprotein lipase) [NCBI Gene 4023] {aka HDLCQ11, LIPD}, RGN (regucalcin) [NCBI Gene 9104] {aka GNL, HEL-S-41, RC, SMP30}, PPARG (peroxisome proliferator activated receptor gamma) [NCBI Gene 5468] {aka CIMT1, FPLD3, GLM1, NR1C3, PPARG1, PPARG2}, NANOG (Nanog homeobox) [NCBI Gene 79923], SOX2 (SRY-box transcription factor 2) [NCBI Gene 6657] {aka ANOP3, MCOPS3}, ACOT2 (acyl-CoA thioesterase 2) [NCBI Gene 10965] {aka CTE-IA, CTE1A, MTE1, PTE2, PTE2A, ZAP128}, POU5F1 (POU class 5 homeobox 1) [NCBI Gene 5460] {aka OCT3, OCT4, OCT4Borf1, OTF-3, OTF3, OTF4}, TMEM26 (transmembrane protein 26) [NCBI Gene 219623], TRIP4 (thyroid hormone receptor interactor 4) [NCBI Gene 9325] {aka ASC-1, ASC1, HsT17391, MDCDC, SMABF1, ZC2HC5}
- **Diseases:** metabolic disorders (MESH:D008659), chronic inflammation (MESH:D007249)
- **Chemicals:** triglyceride (MESH:D014280)

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12873142/full.md

---
Source: https://tomesphere.com/paper/PMC12873142