#mitophagy

[bpod-bpod]

Power Lunch

Around 145,000 people in the UK are currently living with Parkinson’s disease. It’s a progressive and incurable brain disorder that affects movement and causes other issues such as insomnia, dementia and mental health problems. Yet despite years of research, we still understand little about what causes it. One possible culprit could be mitochondria – the small structures inside cells that produce energy. During the normal course of life, worn out mitochondria are ‘eaten up’ through a process called mitophagy (highlighted in orange in this image of mouse kidney tissue) and replaced with healthy new ones. Researchers have discovered that mitophagy doesn’t work properly in brain cells from genetically engineered mice with a version of Parkinson’s and might be causing some of the problems seen in the disease. Excitingly, they have also shown that mitophagy can be restarted using certain chemicals, which could one day be developed into much-needed treatments for patients.

Written by Kat Arney

Image from work by Francois Singh and colleagues

MRC Protein Phosphorylation and Ubiquitylation Unit, University of Dundee, Dundee, UK

Image originally published with a Creative Commons Attribution 4.0 International (CC BY 4.0)

Published in eLife, August 2021

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[currentsinbiology]

Broken mitochondria use 'eat me' proteins to summon their executioners 

When mitochondria become damaged, they avoid causing further problems by signaling cellular proteins to degrade them. In a new study, scientists report that they have discovered how the cells trigger this process, which is called mitophagy. In cells with broken mitochondria, two proteins -- NIPSNAP 1 and NIPSNAP 2 -- accumulate on the mitochondrial surface, functioning as 'eat me' signals, recruiting the cellular machinery that will destroy them.

[currentsinbiology]

Researchers discover novel mechanism linking changes in mitochondria to cancer cell death

To stop the spread of cancer, cancer cells must die. Unfortunately, many types of cancer cells seem to use innate mechanisms that block cancer cell death, therefore allowing the cancer to metastasize. While seeking to further understand cancer cell death, researchers at the University of Notre Dame discovered that the activation of a specific enzyme may help suppress the spread of tumors.

The findings, published in Nature Cell Biology, demonstrate that the enzyme RIPK1 decreases the number of mitochondria in a cell. This loss of mitochondria leads to oxidative stress that can potentially kill cancer cells, though researchers speculate the cancer cells could find ways to shut down this effect.

During the study, the Notre Dame team discovered that when the enzyme RIPK1 is activated in a cell, it can cause the number of mitochondria—considered the "power plants" of the cell—to decrease as the cell consumes its own components for energy, a process called mitophagy. This was surprising, given RIPK1 was well-known to regulate necrosis, a completely distinct cell death mechanism.

More information: Mark A. Hawk et al. RIPK1-mediated induction of mitophagy compromises the viability of extracellular-matrix-detached cells, Nature Cell Biology (2018). DOI: 10.1038/s41556-018-0034-2

[scitechchron]

SciTech Chronicles. . . . . . . . .March 15th, 2026

SciTech Chronicles. . . . . . . . .March 15th, 2026

Vol V Issue 61 Who Said this? When a population is dependent on a machine, they are hostages of the men who tend the machines. Today, 258 li

[stemcelltherapies]

Light-Sensing Eye Cells Can Recover from the Brink of Death

Photoreceptors are the retina's light sensors, and when they die, vision is lost permanently. Scientists have long believed that once these cells begin apoptosis, a controlled form of cell suicide, the process cannot be stopped. New research challenges this assumption, showing that photoreceptors can actually bounce back from the edge of death if the damaging stress is removed. In lab experiments, researchers exposed photoreceptor cells to severe stress that triggered classic signs of apoptosis, including cell rounding and activation of death enzymes. Surprisingly, when the stress was lifted, the cells reversed these changes and survived. The recovery depended on healthy mitochondria, the cell's power plants, and on mitophagy, a cellular cleaning process that removes damaged mitochondrial components. When scientists boosted this recycling process, more cells survived; when they blocked it, the cells died. The team confirmed these findings with temporary retinal detachment, observing photoreceptors recovering from apoptotic damage. The discovery suggests that vision loss from conditions like retinal detachment or macular degeneration might be preventable or reversible if doctors can find ways to trigger this natural recovery mechanism.

Recovery from apoptosis in photoreceptor cells: A role for mitophagy - Cell Death & Disease

Photoreceptors (PRs) are specialized light-sensitive cells responsible for vision, and their death is the primary cause of retinal degenerat

[cancer-researcher]

[medicomunicare]

An UBIquitous Parkin to take a NAP iSINT BAD while OPTN' for cargo hold: but TANK-binding will lead to a mit-o-loss

There are several pathways to induce mitophagy, or the self-degradation of irreversibly damaged cellular mitochondria. The most well-characterized of these depends on proteins called PINK1 and Parkin, two proteins actively involved in the abnormalities of brain cells affected by Parkinson’s disease. Two other proteins, TFEB and HKDC1, play a key role in the maintenance of both mitochondria and…

An UBIquitous Parkin to take a NAP iSINT BAD while OPTN' for cargo hold: but TANK-binding will lead to a mit-o-loss

[cytgen]

Melatonin Improves Left Ventricular Mitochondrial Dynamics in Rats - Cytology and Genetics

There is increasing awareness that efficient and regular mitochondrial dynamics improvement cardiac function and affects the quality of life