This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Autophagy is an important cellular recycling process that degrades misfolded proteins and damaged organelles. In typical (“canonical”) autophagy, membranes derived from the endoplasmic reticulum surround damaged materials that need to be degraded, and the proteins Atg5 and Atg7 help form specialized digestion compartments (autophagosomes), but another type of autophagy, called alternative autophagy, was recently discovered. In alternative autophagy, the membranes that envelop the damaged materials are derived from the trans-Golgi membrane, and Atg5 and Atg7 do not participate in autophagosome formation. Alternative autophagy seems to be activated primarily under conditions of cell stress, and it plays roles in many diseases, such as heart disease, neurodegenerative disease, cancer, inflammatory bowel disease, and bacterial infection..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Reperfusion of heart tissue with blood after interruption of the blood supply (ischemia) often contributes to inflammation and cell death, including a specific form of cell death called pyroptosis, which can be regulated by the protein caspase-4. The protein beclin-1 is involved in an intracellular degradation process called autophagy that can limit cell death. However, whether beclin-1 limits caspase-4-mediated pyroptosis after heart reperfusion injury remains unclear. To find out, a recent study examined the effects of beclin-1 overexpression in mouse hearts and cultured human heart cells subjected to ischemia/reperfusion. Ischemia/reperfusion increased caspase-4 activity and the expression of the pyroptosis protein gasdermin D. In contrast, beclin-1 overexpression decreased caspase-4 activity, gasdermin D expression, and the levels of the inflammation molecule IL-1β..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Recurrent pregnancy loss – two or more losses before 24 weeks of pregnancy – affects 1-2% of pregnant women. Although some factors have been identified, in most cases the cause is unclear. Researchers are focusing on the critical balance between immune cells and the developing embryo at the maternal-fetal interface. Decidual natural killer (dNK) cells, immune cells in the uterus, must use inflammation to promote the formation of the placenta’s blood supply while also maintaining immune tolerance to prevent damaging the embryo. This delicate balance requires another cell type – trophoblasts, embryonic cells that develop into the placenta. Recently, researchers examining trophoblast-dNK crosstalk found that one important pathway was affected in patients experiencing recurrent pregnancy loss. Autophagy regulates degradation of damaged cells, clearing the way for healthy cells to form tissue..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Atherosclerosis (AS), or thickening of the arteries due to plaque buildup, is a common and potentially deadly condition. A procedure called percutaneous transluminal coronary angioplasty (PTCA) has markedly improved patient survival, but narrowing of the arteries after PTCA (restenosis) remains a problem. Unique extracellular vesicles derived from endothelial colony-forming cells (ECFC-exosomes) are known to help repair injured vessels. Therefore, a new study explored the effects of ECFC-exosomes in a human cell model and a rat model of AS-/PTCA-induced vessel injury. In lipid-injured human vascular cells, ECFC-exosomes promoted repair-related processes such as cell proliferation, migration, and tube formation by enhancing autophagy, a process in which intracellular debris is degraded and recycled. Specifically, the exosomal miRNA miR-21-5p inhibited expression of the protein SIPA1L2 to increase autophagy..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Too much dietary fat can be bad for our health. Chronic high lipid intake results in the accumulation of triglycerides in the liver, causing nonalcoholic fatty liver disease (NAFLD). One contributor to NAFLD is the inhibition of a process called autophagy, where the body’s cells clean up intracellular components that are damaged or no longer needed. Unfortunately, how autophagy inhibition results in NAFLD is unknown. A recent study aimed to determine what molecular pathways inhibit autophagy to cause NAFLD. Using yellow catfish as a model, they compared the effects of regular and high-lipid diets on autophagy and lipid metabolism. RNA sequencing showed that a high-fat diet altered the expression of many genes associated with lipid metabolism and autophagy. A pair of proteins, FXR and CREB, served as a switch to regulate these changes, maintaining a proper fatty acid balance and protecting cells from lipid-induced damage..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Autophagy is a critical process in healthy human cells that removes excess organelles and substances while generating energy. But in cancer cells, autophagy can either feed growing tumors—literally supplying energy—or suppress them by clearing out cancer-promoting substances. Recently, researchers examined this process in non-small cell lung cancer (NSCLC) and focused on GNIP1, a TRIM family protein. Other TRIM proteins have been associated with autophagy previously, but this is the first autophagy study to examine GNIP1. GNIP1 expression was elevated in tumor cells from NSCLC patients, and clinically, it was associated with poor prognosis and survival time. Induced overexpression of GNIP1 in cultured NSCLC cells increased the cancerous behaviors proliferation and migration. Additional cell culture experiments indicated that GNIP1 did this by enhancing autophagy. Specifically, GNIP1 mediated the breakdown of the VPS34 complex, an autophagy inhibitor..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Extracellular vesicles (EVs) function in many physiological events ranging from normal cellular activity to pathogenic processes. Some EVs prepared in vitro have exhibited therapeutic effects in preclinical models of immune or neurodegenerative disease. In a recent study, researchers generated EVs enriched with HSPB8 (small heat shock protein B8) in vitro from oligodendroglia (OLs). HSPB8 protects cells from oxidative stress-mediated cell death by supporting autophagic activity and could be carried by EVs. Both the native OL-EVs and the HSPB8-enriched OL-EVs were internalized by a microglial cell line and primary mixed neural cultures without inducing cell death. The HSPB8-enriched OL-EVs increased the endogenous production of HSPB8 mRNA. Both EV subsets helped maintain cellular homeostasis during chronic inflammation by increasing autophagic vesicle formation..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Acetaminophen (N-acetyl-p-aminophenol, APAP) is a commonly used over-the-counter analgesic and antipyretic, but an overdose can cause severe liver damage or even liver failure, and the therapies for such acetaminophen-induced liver injury (AILI) are limited. To search for new treatment targets, researchers recently investigated the roles of the IL-33/ST2 cytokine signaling pathway in a mouse AILI model. Compared to wild-type mice, IL-33-knockout mice had worse hepatotoxicity after acetaminophen overdose, as indicated by greater hepatocyte necrosis, DNA accumulation, and type I IFN production, suggesting that IL-33 signaling normally has a protective effect. Further investigation in liver cell lines revealed that the binding of IL-33 with its receptor ST2 enhanced the interaction of Beclin-1 with the STING C-terminus..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Despite being the standard treatment for lung cancers, immune checkpoint inhibitors (ICIs) are often less effective for patients with EGFR mutations. And these mutations are far from uncommon; 40% of lung adenocarcinoma (LUAD) patients have them, but one protein that might play a role in this process is ARID1A. A recent study examined ARID1A expression in a cohort of LUAD patients with or without EGFR mutations. Overall, low ARID1A expression corresponded to increased immune cell infiltration and longer survival times. The data also suggested that ICIs were more effective for LUAD patients with EGFR mutations if they had low ARID1A expression. Mechanistic experiments in cultured EGFR-mutated LUAD cells suggested that reducing ARID1A expression inhibited autophagy. Autophagy is a normal process in healthy cells, but it helps cancer cells evade the immune system. Specifically, reduced ARID1A expression decreased autophagy by activating the EGFR/PI3K/Akt/mTOR pathway..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"These tiny sacs within cells are called multivesicular bodies, or MVBs. Once considered nothing more than a part of the cell’s waste disposal and recycling system, MVBs are now understood to play multiple important roles, including promoting tumor progression. MVBs selectively load substances such as lipids, proteins, and nucleic acids, and then fuse with the cell membrane to release their payloads outside the cell in the form of exosomes. In tumors, the key proteins involved in MVB formation, transport, and fusion are abnormally expressed, and evidence suggests that MVBs promote virtually all aspects of cancer progression – from tumor expansion to drug resistance. For example, MVBs direct the cellular degradation needed for cancer cells to form the finger-like projections that help them spread to other organs, and studies show that MVB cargoes can transfer cancer drug resistance from one cell to another..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Neddylation is the process by which the molecule NEDD8 is attached to cellular proteins. Elevated neddylation in the body has been linked to various cancers. Inhibiting this protein modification has therefore become a promising anticancer strategy. A new study describes how researchers used this anti-neddylation approach to kill esophageal cancer cells. The team treated lab-grown esophageal cancer cells with MLN4924, a known neddylation inhibitor. They found that MLN4924 indirectly led to the programmed cell death, or apoptosis, of the cancer cells. By reducing neddylation, MLN4924 actually promoted a cell survival mechanism known as autophagy. Autophagy keeps cells healthy and alive by clearing harmful debris. Interestingly, it also gave the researchers access to a “kill switch” for diverting from autophagy to apoptosis. That switch came in the form of the protein ATF3, which can be silenced to cause cell death..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"In individuals with Duchenne muscular dystrophy (DMD), lack of the protein dystrophin impairs autophagy and drastically disrupts myotube development. The PI3K/Akt/mTOR pathway is a vital autophagy-regulating pathway that also participates in skeletal muscle differentiation. However, the precise disruption of this pathway in the context of DMD remains unclear. To clarify the mechanism, researchers recently performed protein profiling on dystrophin-deficient myoblasts. The deficient (dfd13) myoblasts were not able to achieve terminal differentiation. They also exhibited strongly increased PTEN expression and perturbed PI3K/Akt/mTOR regulation. In addition, rictor-mTORC2 was inactivated, which caused FoxO3 misregulation and ultimately increased autophagy-related gene activation. Autophagosome formation was excessive in the dystrophin-deficient myoblasts; however, subsequent LC3B-I to LC3B-II conversion and autophagic flux were decreased, consistent with the known autophagy disruption in DMD..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"One hallmark of neurodegenerative diseases such as Alzheimer's and Parkinson's is protein accumulation in the brain. That accumulation is driven by structural modification of the cellular prion protein. which produces self-generating particles in the brain. Neuronal cell death caused by these protein clusters occurs through autophagy, the body’s way of degrading damaged cells. Unfortunately, the pathways mediating prion-driven autophagy in neurons remain unclear. A recent study evaluated the role of calcium signaling – a common signaling pathway affected by prion proteins. Using neuronal cells from mice, researchers measured calcium signaling and the levels of proteins involved in metabolic stress and autophagy. Their results showed that human prion peptide increased the concentration of calcium in neurons. Inhibiting this prion-mediated calcium uptake in neurons prevented autophagic cell death. and preserved the activity of a protein called AMPK, which is involved in maintaining energy balance in cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"CMTM7 is a tumor-suppressing protein that inhibits the growth of cancer cells in the esophagus and lungs. Studies suggest that CMTM7 suppresses tumor progression by regulating autophagy, the cell’s waste disposal process, but exactly how CMTM7 regulates autophagy has remained unclear. A new study reveals some of the molecular machinery CMTM7 uses to influence autophagy and stop cancer cell growth. Initial experiments on human cancer cells confirmed that overexpressing CMTM7 led to enhanced autophagy while eliminating CMTM7 impaired autophagy. Further experiments showed that CMTM7 interacts with the proteins Beclin1, VPS34, and ATG14L and with the autophagy-associated protein Rab5. This ensemble of molecules—led by CMTM7—works together to promote autophagy in the cell. To examine the resulting effect on tumor growth, researchers eliminated CMTM7 from cancer cells injected into mice. They found that CMTM7 knockdown was linked to an increase in tumor volume and weight..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Rabies causes severe neurological symptoms and has a high mortality rate, killing over 59,000 people each year. Rabies virus encodes five phosphoproteins (P) that are involved in viral genomic replication, transport, oxidative stress, interferon antagonism, and autophagy induction. Unfortunately, the specific functions of each P protein are poorly understood. A recent study zeroed in on the viral protein P5. Using cell lines, researchers found that P5 attaches to the N-terminal residues of the protein beclin1 (BECN1). P5 binding to the ring-like structure of BECN1 induced incomplete autophagy due to incomplete fusion with lysosomes. This process promoted rabies virus replication by increasing the levels of viral proteins. Silencing the gene for beclin1 did not reproduce this pattern of P5-induced viral replication. This study identifies for novel role for P5, whereby P5 binding to the BECN1 ring promotes viral replication by inducing incomplete autophagy..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Rapamycin is a promising candidate as an anti-aging drug. Normally used to fight cancer, rapamycin has been shown to extend the lifespan of mice. But what about humans? To find out, researchers monitored the effect of rapamycin on test tubes of human coronary artery endothelial cells. These cells are integral to the structure and homeostasis of blood vessels in the heart but tend to harden with age, posing a looming threat to older individuals. Experiments showed that while rapamycin suppressed the expression of certain senescence-related proteins, it actually promoted endothelial cell differentiation into mesenchymal cells through morphological changes by activating autophagy, causing a functional modification. Because heart function is supported by the vascular network, induction of the endothelial–mesenchymal transition can drive the pathogenesis of heart disease..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Autophagy is the process by which healthy cells degrade and recycle waste material. Researchers are finding that this vital function is interrupted in different forms of cancer, including brain cancer. A new review describes how researchers are repairing broken autophagy pathways in tumors using microRNAs, or miRNAs. miRNAs are small non-coding RNA molecules that regulate a variety of cellular processes— including autophagy. Understanding the molecular targets of miRNAs and their function is crucial, as it could lead to the development of new therapies for patients with brain tumors..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"The development of solid tumors like melanomas is driven by cancer stem cells (CSCs). These cells can also promote tumor growth, dormancy, metastasis, recurrence, and chemoresistance, which contribute to poor cancer outcomes. An intracellular degradation/recycling pathway called autophagy is thought to regulate the “stemness” of CSCs to enable these effects. To clarify the mechanism, a recent study examined CSCs isolated from human melanoma cell lines. The expression of the molecule Sec23a was lower in the CSCs than in the original melanoma cells, and the reduced Sec23a expression was associated with increased stemness in vitro and tumor growth in vivo, indicating a negative correlation between Sec23a and CSC stemness. Further experiments revealed that Sec23a downregulation increases CSC stemness by promoting autophagy. Specifically, Sec23a downregulation enhances endoplasmic reticulum (ER) stress, which leads to upregulation of the ER stress-responsive protein FAM134B..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"A healthy heart is one that stays in shape—literally. Remodeling of the heart’s structure is both a cause and an effect of heart disease. One molecule that could help fortify the heart against harmful reshaping is STING. STING is a signaling molecule that triggers a fleet of protective chemicals during infection, but recent studies suggest STING could also play a role in heart injury. To explore this role, researchers monitored STING in mouse models of heart remodeling. Mice experiencing heart remodeling showed elevated levels of STING. To isolate the effects of STING, certain mice were genetically altered to overexpress the molecule. Compared with unmodified mice, these high-STING mice showed smaller changes in heart size and better overall heart function. Cell experiments revealed that STING could provide these protective effects by combating autophagy. Autophagy is the process of degrading and recycling parts of the cell and is the driver of heart remodeling..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.

This resource is a video abstract of a research paper created by Research Square on behalf of its authors. It provides a synopsis that's easy to understand, and can be used to introduce the topics it covers to students, researchers, and the general public. The video's transcript is also provided in full, with a portion provided below for preview:

"Temozolomide , or TMZ , is a chemotherapy agent used to treat glioblastoma. TMZ causes DNA damage that results in tumor cell apoptosis and thereby increases the survival rate of patients with glioblastoma. Over time, however, glioblastoma cells can become less responsive to TMZ because the drug induces autophagy in these cells, clearing otherwise toxic cargo and saving the cells from premature death. This chemoresistance can prove fatal for patients who rely on the anti-cancer effects of TMZ. Now, researchers have discovered a way to keep TMZ working long-term: by combining it with the cholesterol-reducing statin simvastatin , or Simva. Previous studies have shown that long-term consumption of statins prior to or in addition to cancer therapeutics can increase the survival rates of patients with different forms of cancer. Simva is shown to be less toxic towards the liver and gastrointestinal tract than other statins and can cross the blood-brain barrier to target glioblastoma cells..."

The rest of the transcript, along with a link to the research itself, is available on the resource itself.