Related Experiment Video

Updated: Jan 23, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
07:40

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy

Published on: May 26, 2023

1.6K

Sonodynamic therapy inhibits palmitate-induced beta cell dysfunction via PINK1/Parkin-dependent mitophagy

Tian Guo1, Tianyang Liu1, Yun Sun1

  • 1Department of Pathophysiology, Harbin Medical University, Harbin, 150081, China.

Cell Death & Disease
|June 13, 2019
PubMed

Insights

Sonodynamic therapy (SDT) protects beta cells from lipotoxicity in type 2 diabetes mellitus (T2DM). SDT promotes mitophagy, improving mitochondrial function and insulin secretion, offering a novel therapeutic approach for T2DM islet protection.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Biomedical Engineering

Background:

  • Type 2 diabetes mellitus (T2DM) involves beta cell dysfunction due to glucose and lipid overload, leading to oxidative stress and inflammation.
  • Current therapies for T2DM often overlook strategies to modulate beta cell function and prevent failure.
  • Lipotoxicity, simulating a high-fat diet, is a key factor in beta cell failure.

Purpose of the Study:

  • To investigate the efficacy of Sonodynamic therapy (SDT) in protecting beta cells from lipotoxicity-induced injury.
  • To elucidate the underlying mechanisms of SDT's protective effects on beta cells.
  • To explore SDT as a potential therapeutic strategy for T2DM islet protection.

Main Methods:

  • Established a beta cell injury model using palmitic acid (PA) to mimic T2DM lipotoxicity.
  • Applied Sonodynamic therapy (SDT) to treat the injured beta cells.
  • Investigated mitochondrial function, reactive oxygen species (ROS) production, inflammatory responses, and insulin secretion.
  • Analyzed the role of PINK1/Parkin-dependent mitophagy and its regulation by SDT.
  • Utilized cyclosporin A (CsA) to inhibit mitophagy and assess its impact on SDT's protective effects.

Main Results:

  • SDT induced transient mitochondrial reactive oxygen species (ROS) production in beta cells.
  • SDT improved mitochondrial morphology and function, inhibited inflammation, and reduced beta cell dysfunction.
  • The protective effects were mediated by PINK1/Parkin-dependent mitophagy, with SDT rescuing PINK1 mRNA transcription.
  • SDT significantly increased insulin secretion from beta cells.
  • Inhibition of mitophagy by CsA abrogated the protective effects of SDT.

Conclusions:

  • SDT effectively protects against lipotoxicity-induced beta cell failure in a T2DM model.
  • PINK1/Parkin-dependent mitophagy is a key mechanism underlying SDT's protective action.
  • SDT enhances mitochondrial quality control and insulin secretion, offering a promising therapeutic avenue for T2DM.
  • This study provides a theoretical basis for using SDT in islet protection strategies for T2DM management.

More Related Videos

Time-Lapse Video Microscopy for Assessment of EYFP-Parkin Aggregation as a Marker for Cellular Mitophagy09:29

Time-Lapse Video Microscopy for Assessment of EYFP-Parkin Aggregation as a Marker for Cellular Mitophagy

Published on: May 4, 2016

7.6K
Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima09:13

Sensitive Measurement of Mitophagy by Flow Cytometry Using the pH-dependent Fluorescent Reporter mt-Keima

Published on: August 12, 2018

15.6K

Related Concept Videos

Feedback Inhibition00:46

Feedback Inhibition

Biochemical reactions are occurring constantly in cells, converting starting substances to different products, usually with the help of enzymes that speed the reactions. Without enzymes, it would take far too long for most reactions to occur to be useful to the cell!
56.9K
Gene Therapy00:59

Gene Therapy

Gene therapy is a technique where a gene is inserted into a person’s cells to prevent or treat a serious disease. The added gene may be a healthy version of the gene that is mutated in the patient, or it could be a different gene that inactivates or compensates for the patient’s disease-causing gene. For example, in patients with severe combined immunodeficiency (SCID) due to a mutation in the gene for the enzyme adenosine deaminase, a functioning version of the gene can be...
27.4K
Frequency-dependent Selection01:21

Frequency-dependent Selection

When the fitness of a trait is influenced by how common it is (i.e., its frequency) relative to different traits within a population, this is referred to as frequency-dependent selection. Frequency-dependent selection may occur between species or within a single species. This type of selection can either be positive—with more common phenotypes having higher fitness—or negative, with rarer phenotypes conferring increased fitness.
23.2K
Enzyme Inhibition01:30

Enzyme Inhibition

Inhibitors are molecules that reduce enzyme activity by binding to the enzyme. In a normally functioning cell, enzymes are regulated by a variety of inhibitors. Drugs and other toxins can also inhibit enzymes. Some inhibitors bind to the enzyme’s active site, while others inhibit enzymatic activity by binding to other sites on the protein structure.
91.7K
Contact-dependent Signaling01:19

Contact-dependent Signaling

Contact-dependent signaling, as the name suggests, requires that communicating cells be in direct contact with each other. This is achieved either through receptor-ligand interactions or by specialized cytoplasmic channels that allow the flow of small molecules between cells. In animal cells, channels called gap junctions facilitate contact-dependent signaling in certain tissues, whereas, plasmodesmata perform a similar function in plants.
Gap Junctions
In animal cells, gap junctions are formed...
46.9K
Induced Pluripotent Stem Cells01:13

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different types of cells. Ordinarily, cells that have differentiated into a specific cell type are post-mitotic—that is, they no longer divide. However, scientists have found a way to reprogram these mature cells so that they “de-differentiate” and return to an unspecialized, proliferative state. These cells are also pluripotent like embryonic stem cells—able to produce all cell types—and are therefore...
27.3K