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:

"Diabetic encephalopathy (DE), a complication of type 2 diabetes (T2D), causes cognitive impairment that increases the chance of death. Because DE has no cure, investigating its mechanisms and finding new therapies are crucially important. DE has similar symptoms to Alzheimer's disease (AD), and both involve elevated β-amyloid peptide and hyperphosphorylated tau protein, so finding new therapies for DE could involve using what's already known about AD. The autophagy-lysosomal pathway (ALP) breaks down persistent proteins in cells and helps clear the neurofibrillary tangles and senile plaques characteristic of AD, and upstream genes called transcription factor EB (TFEB) and mechanistic target of rapamycin (mTOR) regulate ALP. Researchers used both cultured cells and a mouse model of T2D to investigate whether TFEB activation could help alleviate DE. T2D mice showed cognitive impairment and AD-like pathology, which were alleviated when TFEB was activated by either mTOR inhibition or TFEB overexpression..."

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 strongest genetic risk factor for Alzheimer’s disease may impair the body’s cellular recycling system, allowing the build-up of harmful byproducts in the brain. People carrying the gene variant known as APOE4 are at an increased risk for the early development of Alzheimer’s and show high numbers of the brain plaques characteristic of the disease. But the underlying reason for this effect isn’t clear. Now, researchers have shown that APOE4 interferes with autophagy -- the body’s way of recycling unneeded or harmful cellular material – providing new insights into how and why APOE4 conveys such a strong risk for Alzheimer’s. The team looked at the relationship between APOE4 and a protein known as TFEB, considered a master regulator of autophagy-related genes. Prior studies have linked reduced TFEB expression to the presence of amyloid-beta plaques in the brain..."

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:

"Wheat is one of the world’s most important crops. However, wheat production is currently threatened by various fungal diseases throughout the growing season. Fusarium head blight (FHB), caused by _Fusarium graminearum_, is one of the most important fungal diseases of wheat causing serious wheat yield losses, as well as mycotoxin contamination. One approach to combating this type of infection is through autophagy. Autophagy is a highly conserved physiologic process critical for macromolecule turnover, stress response, and survival in eukaryotes and plays an important role in fungal pathogenesis. _Streptomyces hygroscopicus_ S89, a member of the natural wheat microbiota, has shown high efficiency in reducing mycelial growth of _F. graminearum_—possibly through autophagy. Researchers found that the antifungal compound rapamycin secreted by _S. hygroscopicus_ S89 stimulates autophagic flux and affects the acetylome of _F. graminearium_ by promoting the degradation of acetyltransferase Gcn5..."

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:

"Pancreatic neuroendocrine tumors, or PNETs, are a form of cancer that invade the hormone-producing cells in the pancreas. While many are benign, PNETs tend to behave unpredictably. And many treatments against malignant PNETs have proven ineffective. Now, a new study suggests that the anti-inflammatory herbal blend Zyflamend could be a promising treatment option. Experiments showed that Zyflamend reduces cell survival and induces cell death in pancreatic cancer cells in a dose-dependent manner. Zyflamend does so by inducing apoptosis, a programmed death sequence initiated by discarded cells. This form of cell death appears to be mediated by the JNK pathway, an important part of inflammatory responses in mammals. Although more work is needed to understand the full effects of this herbal blend in the clinic. These findings suggest that Zyflamend could be a novel add-on therapy for treating pancreatic cancer..."

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:

"Survival is a complex energy-balancing act that involves a number of cell signaling pathways. One important player in this act is the protein mTORC1. Previous studies have shown that inhibiting mTORC1 is beneficial for health—and lifespan—serving as one promising way to fight cancer, for example. Now, a new computational model could reveal important details about key players in aging. This model captures the dynamic of known key players in the aging process, such as AMPK, mTORC1, and SIRT signaling pathways. Model simulations indicated that PRAS40 can be considered as another mTORC1 inhibitor. This access point is clinically important, as it provides a way of suppressing mTORC1 with the optimum dose of the inhibitor rapamycin, which at high doses and long exposure is known to cause problems such as insulin resistance. Results suggest that Sestrin2 is another potential candidate that can inhibit mTORC1..."

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 an essential intracellular recycling and degradation process. Dysfunction of autophagy is associated with diseases such as cancer, neurodegeneration, and cardiovascular disease. Some of these diseases don’t have effective treatments, underscoring the need for a thorough understanding of autophagy regulation. The protein complexes mTORC1 and mTORC2 are both autophagy regulators. mTORC1’s inhibitory effect on autophagy is well described, but mTORC2’s role is more complex and less understood. For example, mTORC2 can suppress autophagy by activating the proteins AKT and SGK-1. For example, mTORC2 can suppress autophagy by activating the proteins AKT and SGK-1, but promote autophagy by activating the protein PKCα. The activity of mTORC2 itself can also be modulated by upstream factors such as nutrients and intracellular signals and through positive and negative feedback mechanisms involving insulin, mTORC1, and other molecules..."

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:

"Diabetic retinopathy (DR) is a severe ocular complication of diabetes mellitus, affecting over 400 million adults worldwide and causing blindness in millions of them. Neurodegeneration is an early event in DR pathogenesis, preceding clinically detectable vascular damage. One potential cause of neuronal loss in DR is the dysregulated autophagy. Unfortunately, the mechanisms underlying autophagy dysregulation in DR remain unclear. A new study focused on the role of a central signaling molecule in this process, mTOR (mechanistic target of rapamycin) is a ubiquitous molecule that integrates diverse underlying signals to coordinate biological processes. Using a mouse model of DR, researchers found that mTOR-related proteins were upregulated shortly after diabetes induction but were then downregulated. Diabetes-induced neurodegeneration observed in this study was evaluated by an increase of apoptosis markers and a decrease in the total cell number..."

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:

"Liver cancer is the third deadliest cancer worldwide, and effective treatments are limited. But inducing apoptosis, a type of programmed cell death, could aid or replace current treatments. Apoptin is a protein that triggers apoptosis specifically in tumor cells. Apoptin also activates autophagy, or the breakdown of unneeded or damaged cellular components, which can either inhibit or induce apoptosis. However, the cellular mechanisms linking these processes remain unclear. So, researchers recently used cultured liver cancer cells and a mouse model of liver cancer to elucidate those mechanisms. First, they confirmed that apoptin increased apoptosis and autophagy in both the cultured cells and the mice. But they also found that the autophagy it activated was protective, slowing the rate of apoptosis. Mechanistically, apoptin increased the levels of reactive oxygen species (ROS) and activated mitophagy, a mitochondria- specific type of 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:

"Autophagy is a catabolic process in which intracellular components are degraded in lysosomes. Stresses such as nutrient deficiency, hypoxia, and chemotherapy can trigger autophagy, making autophagy relevant to cancer treatment. Autophagy appears to play complex dual roles in cancer immune escape. For example, autophagic degradation of the immune checkpoint protein PD-L1 generally enhances T cell activation and suppresses tumor growth, but cancer cells can encapsulate PD-L1 and another checkpoint protein, CD47, in endosomes to prevent their degradation. In addition, MHC-I/II autophagy enables cancer cell immune escape and inhibits antigen presentation and T cell activation. However, autophagic mitochondrial degradation, termed mitophagy, can improve the antitumor immune response. Therefore, autophagy can positively or negatively affect cancer immune escape, which may depend on the experimental context, and autophagy may synergize with immune cells to regulate cancer immune surveillance..."

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 is a chronic inflammatory process where lipids accumulate along the arterial wall. One key protein in atherosclerosis development is AIBP (Apolipoprotein A-I binding protein). AIBP exists both inside and outside cells, but only secreted AIBP is well characterized in atherosclerosis. A recent study found that AIBP is highly expressed in human and mouse atherosclerotic lesions and that the AIBP was concentrated within the inner membrane of macrophage mitochondria. Macrophages are immune cells that can have pro- or anti-inflammatory phenotypes. The interplay between these phenotypes plays a pathogenic role in atherosclerosis. In this study, blocking the production of AIBP in bone marrow aggravated atherosclerosis and increased macrophage infiltration in a mouse model. This bone-marrow-specific AIBP deficiency increased the cleavage of the protein PINK1 (PTEN-induced putative kinase 1)..."

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