Stokes et al. demonstrate that PARP7 “senses” the levels of nuclear NAD+ during early adipogenic differentiation via an ADP-ribosylation-ubiquitin-proteasome pathway to regulate C/EBPβ-dependent proadipogenic gene expression through p300-mediated H3K27 acetylation. Stabilized PARP7 promotes the binding of C/EBPβ to chromatin genome-wide, enhancing lipid synthesis and adipogenesis in vivo.
But the molecular factors responsible for the onset of Barrett’s esophagus remain poorly understood.
The findings, published in Nature Communications, combined family studies, laboratory experiments and genetically engineered mouse models to identify and understand how genetic defects contribute to disease development.
The team sequenced and analyzed genetic material of 684 people from 302 families where multiple members developed Barrett’s esophagus or esophageal cancer. They discovered that a subset of affected family members carry inherited mutations in a gene called VSIG10L.
“We found that this gene acts like a quality control system for the esophageal lining,” said the lead researcher. “When it’s defective, the cells do not mature properly and the protective barrier in the esophageal lining becomes weak, allowing stomach bile acid to cause tissue changes that enhances the risk of developing Barrett’s esophagus.”
When researchers genetically engineered mice with human-equivalent VSIG10L mutations, they found that the esophageal lining became disrupted structurally and molecularly, according to the author. The study found that when the mice were exposed to bile acid, they developed Barrett’s-like disease over time, effectively replicating the disease’s progression in humans.
These genetically engineered mice also represent the first animal model for Barrett’s esophagus based directly on human genetic predisposition to the disease, the author said.
With VSIG10L shown to be a key gene in maintaining esophageal health, family members can now be screened for genetic variants to identify those at a high-risk of developing Barrett’s esophagus or esophageal cancer. ScienceMission sciencenewshighlights.
Extracellular vesicles (EVs) are tiny biological bubbles that carry nucleic acids and proteins between cells, playing an essential role in tissue repair, neuroprotection and immune health. By isolating the surface proteins of these bubbles, researchers can understand more about their biology and build tools to transform extracellular vesicles into next-generation drugs for cancer, neurological conditions and other diseases.
UC Davis biomedical engineers are using EVs to crack the code of the body’s message system. Their findings are detailed in a paper published in ACS Nano.
“EV-mediated intercellular communication is a very powerful system that controls many physiological and pathophysiological phenomena,” said Aijun Wang, a corresponding author of the new study. Wang is Chancellor’s Fellow and professor of biomedical engineering and surgery. “We know that EVs are therapeutically useful. But how do we define what dictates their functions?”
Drugs made of mRNA have the potential to transform medicine—if only they could get into cells in one piece. Now, University of Connecticut researchers have shown that packaging mRNA like a virus could smuggle it into cells safely, opening up a new way to deliver mRNA into cells to treat diseases such as cancer. Their research is published in the journal ACS Nano.
Messenger RNA (mRNA) is a single strand of ribonucleic acids that tells the protein-making machinery inside cells what to do. Usually RNA strands are made using the DNA blueprints inside a cell’s central nucleus, and then travel out to the protein production areas. Getting a medicinal mRNA into a cell from outside, though, is another matter. Most things trying to enter a cell have to pass through an endosome. An endosome is like a decontamination bubble. Its interior becomes acidic, which activates enzymes that chew up anything potentially dangerous—like foreign RNA.
But many viruses have evolved to hijack this system.
Researchers in Belgium have unveiled a striking chemical reaction in which ripples along a frozen reaction front resemble the rays of a shining star. Publishing their results in Physical Review Letters, Anne De Wit and colleagues at the Université Libre de Bruxelles have shed new light on the patterns that emerge in reaction–diffusion systems, offering fresh insight into how similar structures arise in the natural world.
From forest fires to the spread of infectious diseases, many natural processes involve a “front” forming between two distinct states: be they burned and unburned forest, infected and healthy individuals, or any number of other examples in which one state spreads by consuming another.
Such behavior is often described using reaction–diffusion systems, where local reactions are coupled to transport processes such as diffusion. In the lab, this mechanism can be recreated by injecting a chemical compound into the center of a circular chamber filled with another reactant. If the chemistry is autocatalytic —where one of the reaction products catalyzes its own formation—a circular reaction front will form around the injection point.
Several mental health mobile apps with millions of downloads on Google Play contain security vulnerabilities that could expose users’ sensitive medical information.
In one of the apps, security researchers discovered more than 85 medium-and high-severity vulnerabilities that could be exploited to compromise users’ therapy data and privacy.
Some of the products are AI companions designed to help people suffering from clinical depression, multiple forms of anxiety, panic attacks, stress, and bipolar disorder.
An interesting paper evaluating the challenges faced by the existing generation of AAV vectors and proposing best practices for the future of AAVs in gene therapy. Useful tables of serotype, dose, and outcome are included. [ https://journals.asm.org/doi/10.1128/mbio.02957-25](https://journals.asm.org/doi/10.1128/mbio.02957-25)
Adeno-associated virus (AAV), discovered in 1965 (1), was considered a “biological oddity” and was dubbed as “almost a virus” (2), because it fails to undergo a productive replication in the absence of co-infection with a helper virus, such as adenovirus (3), herpesvirus (4), vaccinia virus (5), or human papillomavirus (6). Infection with the wild-type (WT) AAV infection is also not associated with any known disease in humans. However, following the availability of the complete nucleotide sequence of the WT AAV2 genome (7), molecular cloning (8, 9), and the demonstration of its remarkable ability to integrate site-specifically into human chromosome 19q13.3 (10, 11), sparked a significant interest in AAV, subsequently leading to the development of the first generation of recombinant AAV2 vectors (12, 13), followed by further refinements (14, 15).
Ever since then, interest in AAV vectors has continued to grow exponentially (16–19). The first generation of AAV vectors has been used in at least 700 programs, and there are over 200 currently active Phase I/II/III clinical trials for gene therapy of a wide variety of human diseases. Thus far, seven AAV “drugs”—Luxturna for Leber congenital amaurosis (20–22); Zolgensma for spinal muscular atrophy (23); Hemgenix for hemophilia B (24–27); Elevidys for Duchenne muscular dystrophy (28); Roctavian for hemophilia A (29–32); Beqvez for hemophilia B (33) (Beqvez has now been discontinued); and Kebilidi for aromatic L-amino acid decarboxylase deficiency (34, 35)—have been approved by the US Food and Drug Administration.