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Autophagy

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...

Delivery Pathways to the Lysosome

Delivery Pathways to the Lysosome

Eukaryotic cells use different mechanisms to eliminate toxic waste obsolete and worn-out substances. Lysosomes play a pivotal role in this, and hence, these substances are carried to the lysosome from other parts of the cell and extracellular space through different pathways. The most elaborately studied pathways to the lysosome are the endocytic pathways.
Endocytosis
In endocytosis, the cell membrane takes up macromolecules and particles from the surrounding medium. Clathrin-mediated...

Translocation of Proteins into the Mitochondria

Translocation of Proteins into the Mitochondria

Mitochondrial precursors are translocated to the internal subcompartments via independent mechanisms involving distinct protein machineries called translocases.
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...

Electron Transport Chain: Complex I and II

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
ROS generation is regulated and maintained at moderate levels necessary...

Autophagic Cell Death

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...

Receptor Downregulation in MVBs

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that lead to cell proliferation, migration, and differentiation. Overexpression of EGFR stimulates cells to proliferate. Excessive EGFR...

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Related Experiment Video

Updated: Jun 5, 2025

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

Mitophagy Regulates Kidney Diseases.

Xiaolu Fan¹, Linlin Wu², Fengqi Wang^1,3

¹Research Center of Clinical Pharmacy of The First Affiliated Hospital and Liangzhu Laboratory, Zhejiang University School of Medicine, Hangzhou, China.

Kidney Diseases (Basel, Switzerland)

|December 12, 2024

Summary

This summary is machine-generated.

Mitophagy, the process of clearing damaged mitochondria, is vital for kidney health. Its dysregulation is linked to kidney diseases, offering potential therapeutic targets for treatment.

Keywords:

Acute kidney injury Alport syndrome Chronic kidney disease Mitophagy Parkin

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In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

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Last Updated: Jun 5, 2025

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Visualizing Mitophagy with Fluorescent Dyes for Mitochondria and Lysosome

Published on: November 30, 2022

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

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Published on: August 12, 2018

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

In Vitro and In Vivo Detection of Mitophagy in Human Cells, C. Elegans, and Mice

Published on: November 22, 2017

Area of Science:

Cellular Biology
Renal Medicine
Mitochondrial Dynamics

Background:

Mitophagy is essential for cellular homeostasis by removing damaged mitochondria.
The kidney's high metabolic rate necessitates robust mitochondrial quality control via mitophagy.
Dysregulated mitophagy is implicated in various kidney diseases, including acute and chronic conditions.

Purpose of the Study:

To review the role of mitophagy in kidney disease pathogenesis.
To explore mitophagy regulatory proteins (PINK1 and Parkin) as therapeutic targets.
To summarize current understanding and clinical trial progress for mitophagy-based interventions.

Main Methods:

Literature review of mitophagy mechanisms in renal disease.
Analysis of studies on PINK1 and Parkin in kidney pathologies.
Synthesis of findings related to clinical applications of mitophagy regulation.

Main Results:

Mitophagy is crucial for preventing mitochondrial dysfunction in the kidney.
Altered mitophagy levels are observed across diverse renal diseases.
PINK1 and Parkin are key regulators with therapeutic potential.

Conclusions:

Understanding mitophagy mechanisms offers new avenues for treating kidney diseases.
Targeting mitophagy pathways, particularly PINK1/Parkin, shows promise.
Further research is needed to translate mitophagy-based therapies into clinical practice.