# Boron-Enhanced Mitochondrial Repair: DeepA-I Tissue Regeneration

**Authors:** Beyza Yılmaz, Basak Dalbayrak, Mustafa Kucukali, Pinar Uysal Onganer, Elif Damla Arısan

PMC · DOI: 10.1155/sci5/5343930 · Scientifica · 2025-10-26

## TL;DR

A boron-enriched compound called DeepA-I improves mitochondrial health and accelerates tissue repair by reducing oxidative stress in human and mouse cells.

## Contribution

DeepA-I is introduced as a novel boron-based compound that enhances mitochondrial function and tissue regeneration.

## Key findings

- DeepA-I reduces ROS levels and preserves mitochondrial integrity in HUVEC and MEF cells.
- DeepA-I promotes cell migration and wound closure without inducing cytotoxicity.
- DeepA-I modulates NRF2 and Akt signaling to enhance oxidative stress resistance.

## Abstract

Cellular metabolism is a key regulator of tissue repair and regeneration, with mitochondrial function playing a central role in energy production and cellular homeostasis. Dysfunctional mitochondria, often due to excessive reactive oxygen species (ROS), contribute to oxidative stress, impaired wound healing, and chronic inflammation. This study investigates the therapeutic potential of DeepA-I, a Boron-enriched compound, in enhancing mitochondrial health, reducing oxidative damage, and promoting cellular repair in human umbilical vein endothelial cells (HUVEC) and mouse embryonic fibroblasts (MEF). Boron quantification via inductively coupled plasma optical emission spectroscopy (ICP-OES) confirmed its presence in DeepA-I. Cytotoxicity assessment (MTT assay) demonstrated its safety, while fluorescence microscopy (DAPI, MitoSPY, DCFDA) revealed reduced ROS levels and preserved mitochondrial integrity. A scratch assay showed accelerated cell migration and wound closure in DeepA-I-treated cells. Western blot analysis indicated the downregulation of Akt (a proliferation marker) and the upregulation of NRF2, a key regulator of oxidative stress resistance, without affecting apoptosis-related proteins. These results suggest that DeepA-I, via its Boron-mediated mechanisms, enhances mitochondrial function, mitigates ROS-induced damage, and improves tissue repair, positioning it as a promising therapeutic candidate for inflammatory and degenerative conditions.

## Linked entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207], GABPA (GA binding protein transcription factor subunit alpha) [NCBI Gene 2551]
- **Chemicals:** Boron (PubChem CID 5462311)
- **Species:** Homo sapiens (taxon 9606), Mus musculus (taxon 10090)

## Full-text entities

- **Genes:** AKT1 (AKT serine/threonine kinase 1) [NCBI Gene 207] {aka AKT, PKB, PKB-ALPHA, PRKBA, RAC, RAC-ALPHA}, NFE2L2 (NFE2 like bZIP transcription factor 2) [NCBI Gene 4780] {aka IMDDHH, NRF2, Nrf-2}
- **Diseases:** Cytotoxicity (MESH:D064420), degenerative conditions (MESH:D019636), chronic inflammation (MESH:D007249)
- **Chemicals:** DCFDA (MESH:C029569), MTT (MESH:C070243), DAPI (MESH:C007293), ROS (MESH:D017382), Boron (MESH:D001895), DeepA-I (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Cell lines:** vein — Homo sapiens (Human), Finite cell line (CVCL_3722), MEF — Mus musculus (Mouse), Finite cell line (CVCL_9115)

## Full text

_Full body text omitted from this summary view._ Fetch the complete paper as Markdown: https://tomesphere.com/paper/PMC12580037/full.md

## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12580037/full.md

## References

39 references — full list in the complete paper: https://tomesphere.com/paper/PMC12580037/full.md

---
Source: https://tomesphere.com/paper/PMC12580037