Hyaluronic acid ameliorates intervertebral disc degeneration via promoting mitophagy activation

Frontiers in Bioengineering and Biotechnology, 2022 · DOI: 10.3389/fbioe.2022.1057429 · Published: December 16, 2022

Simple Explanation

This study investigates how hyaluronic acid (HA) affects intervertebral disc degeneration (IDD) by looking at its role in promoting mitophagy, a process where cells remove damaged mitochondria. The research examines the effects of HA on nucleus pulposus cells (NPCs) and its potential to protect mitochondria from oxidative stress, a major factor in IDD. The study also seeks to uncover the specific mechanisms by which HA activates mitophagy and protects mitochondrial function in NPCs, potentially leading to new treatments for IDD.

Study Duration

Not specified

Participants

8 patients (4 female, 4 male, age 46–65 years) undergoing lumbar degenerative diseases

Evidence Level

Not specified

Key Findings

1
Hyaluronic acid (HA) can protect mitochondrial function through activation of mitophagy in nucleus pulposus cells (NPCs).
2
C1QBP is involved in HA promoting mitophagy and protecting NPCs from oxidative stress.
3
HA can ameliorate mechanical stress-caused cell apoptosis and ECM degradation by mitophagy activation.

Research Summary

This study found that HA treatment induces mitophagy in NPCs, preventing ROS overproduction and mitochondrial impairment, which subsequently inhibits cell apoptosis, senescence and ECM degradation via the C1QBP signaling pathway under oxidative stress conditions. The protective effects of HA against MS induced NPCs apoptosis and ECM degradation via mitophagy activation were confirmed in an IVD organ culture model. HA promotes mitochondrial dynamics and regulates mitophagy in NPCs by enhancing C1QBP.

Practical Implications

Therapeutic Potential

Hyaluronic acid (HA) shows promise as a therapeutic agent for intervertebral disc degeneration (IDD) by promoting mitophagy and protecting mitochondrial function in nucleus pulposus cells (NPCs).

Mechanism Elucidation

The study identifies C1QBP as a key protein involved in HA-mediated mitophagy, providing a potential target for future therapeutic interventions.

Clinical Applications

The findings support the clinical application of HA in the prevention and treatment of IDD, offering a potential non-surgical approach to managing disc degeneration.

Study Limitations

1
The selected HA concentration of 1 μmol/L may not be the optimal concentration to induce mitophagy in NPCs.
2
The precise molecular mechanisms of C1QBP in HA promoting mitophagy need to be furtherly elucidated.
3
The ex vivo IVD organ culture model and one-strike loading model used in our study were subjected to acute mechanical stress, which is non-physiological and not reflective of IDD mechanism.

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