#autophagy — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #autophagy, aggregated by home.social.
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Reversible suppression of autophagy in a mouse model reveals neuronal resilience.
Japanese researchers created a unique mouse model in which autophagy could be rapidly switched off and restarted using doxycycline. Just four weeks after autophagy was stopped, protein aggregates accumulated in neurons, protein and RNA composition was disrupted, axonal swellings appeared, and the animals developed motor and cognitive impairments.
However, the next stage of the experiment proved most unexpected: after autophagy was restored, most of these changes disappeared. Neurons were cleared of toxic debris, synapse and axon structure was restored, and the mice again successfully passed memory and motor coordination tests.
This study demonstrates that even after significant disruption of cellular homeostasis, nervous tissue retains significant potential for recovery if intracellular degradation mechanisms are reactivated.
If you clutter your house for too long and don't throw out everything that's broken, it will seem like it's no longer fit for habitation. But: clean it, tidy it up, and it'll be as good as new :)#science #cellular_biology #neurology #brain #autophagy #biology
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#ExerciseForHealth #Autophagy #Wellness #HealthyHabits #FitnessMotivation #Biohacking #CellularHealth #WellnessLifestyle #WellbeingJourney #HealthyAging #WellnessCommunity #WellnessGoals #EmotionalWellbeing #WellnessWarrior #PhysicalWellbeing https://mastodon.social/@biohackingpathway/116831006796406543
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TRIM21 induces selective #autophagy of viruses & bacteria.
TRIM21 drives antibody‑directed #xenophagy , rapidly ubiquitinating pathogens & routing diverse viral & bacterial cargo to lysosomes.
#innateimmunity #immunity #microbiology #immunology
https://davidojcius.blogspot.com/2026/06/trim21-induces-selective-autophagy-of.html
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Subject: Fasting, health, and low-calorie feast. Hopefully, this post will be useful to others seeking to lose weight and improve quality of life.
Illustration: The photo shows my first meal after a 3-day water fast [and the only meal for that day]. It took me most of the day to eat it. Note the protein. It's important for reasons explained below.
Surprisingly, the feast in the photo adds up to only 1,700 calories. That's low enough for me to lose weight on, but I'll try to get it down to the 1,200 to 1,650 calories range as frequently as possible. Regardless, as the photo shows, if you'd like to diet, you don't need to starve.
In 2013, I was referred to as "gaunt". Just a year later, I was seriously overweight. I've been up and down since then. I'm approaching age 70 and overweight at that age means deceased. It's time to stabilize to a reasonable weight.
I completed a 3-day [77 hour] water fast today. The fast ran from about 9:00am PT on Sunday [May 24, 2026] to 2:00pm PT on Wednesday [May 27, 2026]. Note: I'd had no food since Saturday, but I did have a bottle of orange Gatorade about an hour before I started the 77 hours.
A water fast is, ideally, a minimum of 72 hours during which you consume only water. It can go to 4 to 5 days, but even just 3 days is risky. This type of fast can have major benefits, but it can also lead to damage or, in some cases, death. It's safer to limit it to 3 to 4 days.
Positive effects can include temporary #autophagy, #ketosis, and improved immune response and #insulin sensitivity. Autophagy is a cellular repair step. Ketosis means, essentially, "burn fat". In short, a water fast can be a thumbs up for weight loss and health in general.
However, negative effects can include a condition called refeeding syndrome, which is potentially fatal; keto flu, which can include headaches, nausea, dizziness, and vomiting; loss of muscle tissue in addition to fat; and strain on the cardiovascular system that can cause damage.
Muscle tissue loss can be reduced, to some extent, by temporarily increasing protein intake immediately after a water fast.
An additional catch is that, after a fast of any type, one can't eat too much in the way of processed foods such as fast food or lost weight will come right back.
In my case, my fast was 100% water during the 77 hours except for a bottle of diet cola. A review shows that, even though diet cola has zero calories, it can interfere with the benefits of fasting. So, I'll try to skip the drink next time.
I took non-gummy multivitamin tablets one day as well. The non-gummy type has zero calories, but I'll probably skip vitamins as well during future fasts as this is advised.
Oddly, I wasn't conscious of hunger at any stage. Towards the end, I did imagine a turkey wing. I think that there were other side effects during the fast, but I'm not certain.
I plan to repeat the fast periodically. I'll do 3 days on the fast and a number of days eating; then repeat the cycle. During eating days, I'll try to minimize processed foods, especially fast food. I figure, perhaps one restaurant meal for every 1 or 2 cycles. We'll see how it goes. In the end, perhaps I'll have a workable long-term Coder Diet.
My first post-fast meal this time, and the only meal for the day [Wednesday, May 27, 2026] is shown in the attached photo.
The meal is a large turkey wing, 275g sliced ham, 1.5 lbs of grape tomatoes, 9 baby potatoes, 4 large carrots, 3 green onions, 5 sweet mini-peppers, 4 small plums, 2 nectarines, and 1 medium honeycrisp apple. The beverage is water with a small amount of rice vinegar added.
I ended up not eating the apple at the time. Estimated calories for the rest: 1,700 calories. Estimated cost for the rest: $24.00. Note: About 70% of the cost came from the meat and the 1.5 lbs of grape tomatoes.
One take-away is that baby potatoes, sweet mini-peppers, carrots, apples, small plums, and especially green onions are all major bargains from both a cost and a calories perspective. Green onions are practically free in both contexts.
#diet #fasting #health -
Stop late-night snacking! 🚫🍔 The 3-Hour Rule activates Autophagy and lets Sirtuins repair your DNA. Become biologically younger overnight. All the facts from the Northwestern University study in the video. #Autophagy #Longevity #HealthyAging #Biohacking
https://www.youtube.com/watch?v=C81IqIxnaWM&list=PLCFAL8lW1qRc2_ByG_7s4bc6h4hcK19_b&index=1
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#OnThisDay The #DavisCup competition, premier international team event in men's tennis, was established (1900)
Happy Birthday Australian #Cricketer Glenn McGrath (1970) - considered one of the greatest bowlers in cricketing history.
Happy Birthday Yoshinori Ohsumi (1945). He discovered of mechanisms for #Autophagy - the process that cells use to destroy and recycle cellular components and received the 2016 Nobel Prize in Physiology or Medicine for his discovery.
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Open position: Postdoc position (Wellcome Trust funded): Structural Basis of #Autophagy Initiation. #science #career #jobs #sciencejobs #job #jobsearch #postdoc www.lifescience.net/jobs/219507/...
Postdoc position (Wellcome Tru... -
#Genetics #Genomics #Academia #AcademicChatter
Technology is bonkers. We've got an #autophagy project that's been going on, oh I don't know, maybe 2.5 years at this point. Or three? Maybe three years. Quite a bit of RNA-Seq involved with three conditions in primary cells.
I just did some quick tallying. 45 samples. About 2.08 billion reads.
2009 me would be flabbergasted at the amount of sequencing. Now it's just how things are.
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`..phosphorylation of Optineurin by TBK1 induces the formation of filaments that phase separate upon binding to linear polyubiquitin.. the condensation of filamentous Optineurin with ubiquitylated cargo promotes the nucleation of cargo and its subsequent alignment with LC3-positive nascent autophagosomes, suggesting that co-condensation processes ensure directionality in selective autophagy`
https://advanced.onlinelibrary.wiley.com/doi/10.1002/advs.202509927
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`Acting as a molecular glue, spermine orchestrates in vivo condensation of α-synuclein, influences condensate mobility, and promotes degradation via autophagy, specifically through autophagosome expansion. This study unveils the interplay between spermine, protein condensation, and functional outcomes, advancing our understanding of neurodegenerative diseases and paving the way for therapeutic development.`
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Fasting benefits WITHOUT starving? 🤯
An innate substance reduces inflammation by 75%. The key: An olive oil ingredient activates the AMPK switch! Goodbye myths, hello science. Your 3-step cell reset plan. 🔑
Watch now: [https://www.youtube.com/watch?v=-JLWPvqnHsQ&list=PLCFAL8lW1qRc2_ByG_7s4bc6h4hcK19_b&index=1]
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Here's one I've been meaning to feature as a #ThursDeath for a while. I'm always down for more gross, grody death metal, so we have to talk about Portland, Oregon's AUTOPHAGY and their debut LP from 2022, 'Bacteriophage'. Over these 9 tracks, there are endless grotesque, churning OSDM style riffs, tons of drum dynamics, and those cavernous, deep, guttural vocals. Hope we get another from these guys soon. A masterful record.
https://autophagypdx.bandcamp.com/album/bacteriophage
#metal #DeathMetal #PortlandMetal #OregonMetal #Autophagy #2022Records #2022Albums #OSDM @HailsandAles @brian @swampgas @rtw @guffo @Kitty @c0m4 @flockofnazguls
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Autophagy, The Gut's Role and Ivermectin in Parkinson's Disease Parkinson's disease is a neurological disorder in which neurons and dopamine-producing cells in your brain begin to die. ...
#anti-aging #autophagy #brain #health #detoxification #fasting #ivermectin #parkinson's #disease
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Autophagy: Gobbles up Viruses and Bacteria, No Pills Required Autophagy literally means "self-eating" and refers to your body's process of eliminating damaged cells by digesting them. I...
#anti-aging #autophagy #fasting #mercola
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Cell Reset NO Hunger? 🤯 Study shows: 75% less inflammation via a naturally occurring compound! Your anti-aging leverage might be in your kitchen (Olive Oil!). 🌿 Food = Information. Switch on your Autophagy. 👇 [https://www.youtube.com/watch?v=LpauESlu9Fg&list=PLCFAL8lW1qRcg33UuQIxYHOaTQX12LurR&index=1]
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Fully Funded PhD in Cancer Biology & Therapeutics
Hebrew University of JerusalemSee the full job description on jobRxiv: https://jobrxiv.org/job/hebrew-university-of-jerusalem-27778-fully-funded-phd-in-cancer-biology-therapeutics/
#autophagy #BasicdrugDiscovery #cancer #mitochondria #ScienceJobs #hiring #research
https://jobrxiv.org/job/hebrew-university-of-jerusalem-27778-fully-funded-phd-in-cancer-biology-therapeutics/?fsp_sid=1579 -
Fully Funded PhD in Cancer Biology & Therapeutics
Hebrew University of JerusalemSee the full job description on jobRxiv: https://jobrxiv.org/job/hebrew-university-of-jerusalem-27778-fully-funded-phd-in-cancer-biology-therapeutics/
#autophagy #BasicdrugDiscovery #cancer #mitochondria #ScienceJobs #hiring #research
https://jobrxiv.org/job/hebrew-university-of-jerusalem-27778-fully-funded-phd-in-cancer-biology-therapeutics/?fsp_sid=333 -
From Synapses to DNA Repair: The Science of Brain Health and Cellular Survival
#CellBiology #Neuroscience #Mitochondria #OxidativeStress #Autophagy #Neurodegeneration #DNARepair #Epigenetics #BrainHealth #BiologyExplained #Neurons #CalciumSignaling #Neuroplasticity #CellDeath #MolecularMedicine
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#Autophagy maintains cellular homeostasis by selectively degrading cytoplasmic cargoes; defects in this pathway can lead to #proinflammatory disease. This study shows that selective degradation of the #immunoproteasome regulates innate inflammatory signaling #PLOSBiology https://plos.io/49FpyKB
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#Adipocyte #autophagy limits gut #inflammation by controlling #oxylipin and #interleukin IL-10
Katja Simon and coworkers
https://www.embopress.org/doi/10.15252/embj.2022112202 -
For #ThrowbackThursday, an episode of the #EMBOPodcast that aired this summer:
Orian Shirihai tells the story of a classic @embojournal paper on the mitochondrial life cycle.
The episode, "Fuse or Die" highlights the importance of my personal nemesis, the well-organised lab notebook.
#mitochondria #autophagy #NeurodegenerativeDisease #mitophagy #HistoryOfScience
https://www.embo.org/podcasts/fuse-or-die-a-conversation-with-orian-shirihai/
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How Mitochondrial Dynamism Orchestrates Mitophagy
Authors Orian S. Shirihai, Moshi Song, Gerald W. Dorn II
Understanding the Significance of Mitochondrial Fission and Fusion
Mitochondrial dynamics refers to the movement of #mitochondria within a cell. This includes #fission, which is when mitochondria divide into two parts, #fusion, which is when two mitochondria join together, and #translocation, which is when mitochondria move from one part of the #cell to another. This movement is important for maintaining the stability of the mitochondrial #DNA, which is the genetic material found in mitochondria, and for controlling the cell's #respiration. It can also be involved in programmed #CellDeath. In the #heart, mitochondrial dynamics #protein s, such as #mitofusin s, optic #atrophy, and dynamin-related protein, are highly expressed and play an important role in maintaining the quality of the #mitochondria. Other roles for mitochondrial dynamics proteins in the #heart include helping to move #calcium into the mitochondria and regulating the structure of the mitochondria.
#Mitochondria are organelles in cells that are responsible for producing #energy. They can change their structure by breaking apart (#fission) and reforming (#fusion). This process is complicated and energy intensive, so it is important to understand why it is necessary. One reason may be that when cells divide, the mitochondria need to be divided equally between the two daughter cells. This requires the #mitochondria to be broken apart and then reformed in each daughter #cell. This process of breaking apart and reforming is more efficient than growing and budding the mitochondria. To help explain this process, the authors use the analogy of an army. Each soldier in the army is like a protein in the mitochondria, and the different units of the army are like the different parts of the #mitochondria. To increase the size of the army, units are added, rather than individual soldiers. This is similar to how mitochondria are modified, by adding or subtracting intact functional units, rather than individual #protein s.
Mitochondria are #organelle s in cells that can change their physical structure by undergoing fission. Fission can be symmetrical, which is when mitochondria replicate and expand the number of #mitochondria in the #cell, or asymmetrical, which is when damaged components of the mitochondria are removed. The major #protein that helps with mitochondrial fission is called Drp1. It is mostly found in the #cytosol, but it needs to be recruited to the outer mitochondrial #membrane to help with fission. Different factors can cause Drp1 to be recruited, such as phosphorylation by mitotic kinase cyclin B–cyclin-dependent-kinase (cdk) 1 complex during #cell division, or interacting with Bcl-2–associated protein x during #apoptosis. Inhibiting Drp1 can protect cells from some, but not all, forms of programmed cell death.
Mitochondria, which are organelles in cells, can be partitioned in #mitosis. The most efficient way to do this is by dismantling and then reconstituting the cellular #mitochondria network through sequential #organelle fission, distribution, and refusion. To explain this concept, the text uses an analogy of how military units are constituted and managed within an army's hierarchical organization structure. In this analogy, each soldier represents an individual respiratory complex #protein, which are grouped together to form a squad (analogous to a respiratory complex). Squads are arranged into platoons, and approximately 6 platoons comprise a functional unit, the company (like 1 complete respiratory chain). The text suggests that it would be easier to add prefabricated supercomplexes to preexisting ones, as by fusing mitochondrial cristae, rather than trying to make a larger or different shaped mitochondrion through the wholesale incorporation of individual proteins. This is because making major structural modifications of respiratory supercomplexes on paracrystalline cristal membranes would first require destabilizing the #membrane, then incorporating additional individual #protein components, and finally reconstructing the original highly organized structure, which is complicated and potentially disruptive.
#Mitochondria are small organelles in cells that can change their physical structure by undergoing fission. Fission can be symmetrical, which means the #mitochondria are split into two equal parts, or asymmetrical, which means the mitochondria are split into two unequal parts. Symmetrical fission is used to replicate and expand the number of mitochondria in the #cell, while asymmetrical fission is used to remove damaged mitochondria from the cell. The major #protein responsible for mitochondrial fission is called Drp1. Drp1 is mostly found in the cytosol, but it needs to be recruited to the outer mitochondrial #membrane to promote fission. Different factors can stimulate Drp1 to move to the outer mitochondrial #membrane, such as phosphorylation by mitotic kinase cyclin B–cyclin-dependent-kinase (cdk) 1 complex. In addition, the endoplasmic reticulum (ER) is often found at the sites of mitochondrial fission. If Drp1 is not present, the mitochondria can still fragment during #mitosis, suggesting that there are other mechanisms that can promote mitochondrial fission.
The text is talking about the process of mitochondrial fission, which is a process that involves connecting and separating parts of a #mitochondria. The author uses the metaphor of making sausage links to explain the process, but then goes on to explain that mitochondria are actually more like a turducken, which is a dish made of a chicken stuffed inside a duck stuffed inside a turkey. This creates layers of poultry, which is similar to the double #membrane /double space structure of #mitochondria. The author then explains that the process of mitochondrial fusion involves connecting the two mitochondria layer by layer, using proteins called mitofusins. Mitofusins have a #GTPase domain, two hydrophobic heptad repeat coiled-coil domains, and a small hydrophobic transmembrane domain. These proteins insert into the outer #membrane of the #mitochondria, and can interact with other proteins in the cytosol. The process of mitochondrial fusion is GTP-independent and reversible, but #GTP #hydrolysis is essential for irreversible outer membrane fusion.
#Mitofusins are proteins that are essential for the first two stages of mitochondrial fusion, which is the process of two mitochondria joining together. This process is important for the exchange of information between the #mitochondria and the #cell. If the mitofusins are deleted or suppressed, the mitochondria become abnormally small and are unable to undergo normal fusion. This can have serious implications for the health of the #cell.
Membrane-by-membrane mitochondrial fusion is a process that helps to keep the structure of the inner and outer membranes of #mitochondria intact. This helps to preserve the process of oxidative phosphorylation, which is important for providing energy to cells. Without this process, molecules that can be toxic to cells can form and interrupt the electron transport chain. This process is also important for maintaining the normal shape of the crista, which is necessary for the proper assembly and functioning of electron transport chain supercomplexes. In addition, it has been shown that interrupting Mfn-mediated OMM fusion can cause a #cardiomyocyte ER stress response, while interrupting Opa1-mediated IMM fusion can compromise mitochondrial function.
Mitochondrial fission and fusion are important processes in #biology, as evidenced by the fact that mutations in genes related to these processes can cause serious diseases in humans. Altering the balance between fission and fusion can have an effect on the shape of #mitochondria, with more fusion leading to longer, more interconnected mitochondria, and more fission leading to shorter, less interconnected mitochondria. It is generally thought that more interconnected #mitochondria are healthier, but this is not always the case. In some cases, mitochondrial #fragmentation can be beneficial, and it is important to understand the interplay between mitochondrial fragmentation and other processes, such as #mitophagy, in order to understand the effects of mitochondrial fission and fusion.
Mitophagy is a process by which cells eat their own #mitochondria. Mitochondria are organelles that produce energy in the form of #ATP, which is used to power most biological processes. Over time, mitochondria can become damaged and produce toxic levels of reactive oxygen species ( #ROS ). To protect the #cell from this damage, it has developed a sophisticated system to identify and remove these dysfunctional #mitochondria. This process is called mitophagy. #Mitophagy is a combination of the words mitochondria and #autophagy, which means "self-eating". It is a way for cells to selectively target and remove damaged mitochondria, while still keeping healthy ones. This helps to maintain the balance between having enough energy-producing #mitochondria and getting rid of the ones that are no longer functioning properly.
Pulse chase experiments are a type of scientific experiment used to study the behavior of molecules over time. In this particular experiment, researchers found that when #mitochondria (the energy-producing organelles in cells) are targeted for #mitophagy (a process of removing damaged mitochondria from the cell), they have a relatively depolarized #membrane potential before being removed. This means that the #mitochondria have a lower electrical charge than normal, and they are less likely to be involved in #fusion events (when two mitochondria join together). The time between the mitochondria becoming depolarized and being removed from the cell can range from less than an hour to about three hours, suggesting that there is a population of preautophagic #mitochondria (mitochondria that are about to be removed). This #preautophagic pool helps to explain the variation in mitochondrial #membrane potential in different cell types. The process that feeds mitochondria into the preautophagic pool is important for determining how quickly #mitochondria are removed from the #cell. Scientists have developed a technology to label individual mitochondria and track their #membrane potential, which has allowed them to identify the event at which depolarized #mitochondria are produced. This event is called asymmetrical fission, and it occurs when the daughter mitochondria produced by the fission event have different #membrane potentials - one daughter has a higher membrane potential than the mother mitochondrion, while the other daughter has a lower membrane potential. This process of asymmetrical fission helps to separate damaged components from healthy components before they are removed from the #cell.
The concept of mitochondrial fission and fusion and how it affects mitochondrial quality. It suggests that when the fusion factors Mfn1 and Mfn2 are both absent, unusually small and degenerated #mitochondria accumulate in adult mouse hearts. This was associated with impaired #cardiomyocyte respiration, but not with measurable alterations in #oxygen consumption. It was later discovered that the isolation procedure used was not capturing the fragmented #mitochondria produced by interrupting mitochondrial fusion. This led to the discovery that Mfn2 is essential to #Parkin-mediated #mitophagy, which is a process that helps to maintain mitochondrial quality. Three recent papers have also implicated the mitochondrial fission protein Drp1 in cardiac #mitophagy, and it is suggested that if asymmetrical mitochondrial fission normally precedes mitophagy, then chronic suppression of fission by ablating Drp1 would have different consequences on #mitophagy depending on when it is assayed.
Mfn2 and PINK1–Parkin Mitophagy Signaling is a mechanism for controlling the quality of #mitochondria in the body. #PINK1 and #Parkin are proteins that are linked to #Parkinson's disease, and mutations in their genes were the first to be identified as causing the disease. Scientists have studied how PINK1 interacts with Parkin, and how this interaction can lead to the destruction of damaged #mitochondria, which is called #mitophagy. #PINK1 is like an ignition switch that senses when mitochondrial damage has occurred, and then activates Parkin-mediated mitophagy. PINK1 is normally not present in healthy #mitochondria, but when mitochondrial damage occurs, PINK1 accumulates and triggers the destruction of the damaged #mitochondria.
PINK1 is a protein that accumulates on damaged mitochondria and helps to promote mitophagy, which is the process of getting rid of damaged mitochondria. PINK1 does this by inducing the cytosolic protein Parkin to move to the mitochondria and ubiquitinate proteins on the outer membrane of the mitochondria. This helps to prevent the spread of damage from the damaged mitochondria to the healthy ones. PINK1 also inhibits the fusion of the damaged mitochondria. There are different theories about the biochemical events that cause Parkin to move to the mitochondria and stop the fusion. It is thought that PINK1 phosphorylates Parkin on certain sites, which helps Parkin bind to the mitochondria. It is also thought that PINK1 phosphorylates ubiquitin, which helps Parkin bind to the mitochondria and ubiquitinate proteins on the outer membrane. Finally, it is thought that PINK1 phosphorylates Mfn2, which helps Parkin bind to the mitochondria and ubiquitinate proteins on the outer membrane. All of these processes help to promote mitophagy and prevent the spread of damage from the damaged mitochondria to the healthy ones.
#PINK1 is a protein that plays an important role in a process called #mitophagy, which is a form of quality control for mitochondria. Mutations in the #PINK1 #gene have been linked to hereditary #Parkinson's disease in humans, but when the PINK1 gene is deleted in mice, it does not cause the same #neurodegenerative pattern seen in humans. Even when the genes for PINK1, Parkin, and DJ-1 are all deleted in mice, it still does not cause the same loss of dopaminergic #neuron s seen in #Parkinson's disease patients. This suggests that there may be other pathways that can compensate for the loss of #PINK1 and #Parkin, such as increased transcription of other E3 #ubiquitin ligases in the hearts of Parkin-knockout mice.
The text is discussing the idea of mitochondrial quality control pathways, which are processes that help keep mitochondria healthy. The text is suggesting that there may be alternate pathways that can be used to maintain mitochondrial health, rather than waiting until the mitochondria are completely depolarized before triggering their removal. It is comparing this idea to the idea of maintaining a car, where it is better to perform regular maintenance and repairs rather than waiting until the car is completely broken down before replacing it.
Like a car, mitochondria can be maintained through preventative maintenance, such as replacing worn parts, and that more serious damage can be repaired by removing and replacing individual components. It also suggests that, like a car, #mitochondria can be repaired by removing and replacing damaged parts, but on a smaller scale. The different types of maintenance and repair may be part of a continuum, rather than distinct categories.
#Mitophagy and mitochondrial dynamism are two processes that are closely connected. Mitophagy is the process of removing damaged #mitochondria from the #cell, while mitochondrial dynamism is the process of mitochondria fusing together and separating. The two processes work together to keep the cell healthy by eliminating damaged mitochondria and preventing healthy mitochondria from being contaminated by the damaged ones. The protein #Mfn2 plays a role in both processes, acting as a factor for mitochondrial fusion when it is not acted on by #PINK1 and as a receptor for #Parkin when it is. This suggests that the two processes are mutually exclusive, meaning that they cannot happen at the same time. This helps to protect healthy #mitochondria from being contaminated by the damaged ones. Finally, the involvement of PINK1 and Parkin in multiple mitochondrial quality control mechanisms shows that there are multiple ways to keep the #mitochondria healthy, which is important for preventing chronic degenerative diseases and providing opportunities for #therapeutic intervention.
