Opinion: We published in Nature Medicine in 2025 for free. In 2026, it cost us $12,850

In June 2025, I led a study that was accepted for publication in Nature Medicine. The cost to publish this manuscript, which reported the results of a randomized clinical trial, was zero dollars. The paper underwent rigorous peer view and extensive edits and copy editing by the editorial staff. This study was the result of years of work by a large team of staff and investigators at Johns Hopkins and was funded by a combination of philanthropy and grants from the National Institutes of Health (your and my tax dollars).

In 2026, I was part of a group that published in Nature Medicine a different NIH-funded study — also the results of years of hard work supported by your and my tax dollars. To comply with the 2024 NIH Public Access Policy that went into effect on July 1, 2025, we paid $12,850 to the publisher. This charge was for open-access fees, now required by the publisher, and was non-negotiable.

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App-Controlled “Wound Zipper” Aids Bespoke Skin Healing

A biomechanical device controlled through a smartphone can quickly close complex wounds, with preclinical research showing it can encourage healing and reduce scarring.

The multi-axis stretchable wound zipper (MSWZ) shrinks and responds like human skin to enable personalized fast and precise healing at a molecular level.

The device, outlined in Advanced Science, mechanically stretches and contracts wounds in multiple directions through a smartphone app and it was able to heal to complex wounds in rats.

The zipper supported matrix remodeling to reduce the risk of scar formation and encouraged blood flow to supply energy and nutrients for optimal healing.

Researcher Yiming Zhang, PhD, from Xinqiao Hospital in Chongqing, China, said it addressed the limitations of conventional surgical sutures or skin staples that only contract in a single direction without being able to manage the force applied.

“We believe this technology offers an innovative solution for future wound care, ultimately alleviating patient suffering and significantly accelerating the healing process,” he said.

The multi-axis wound zipper is engineered from electro-thermally driven mechanical metamaterials and is encapsulated between two layers of polyurethane dressing before use.

It is constructed from a lattice based on nickel-titanium shape-memory alloy that can freely stretch in six directions, spaced 60 degrees apart. This enables it to conform to complex wound morphologies, with precise, programmable mechanical contraction possible through the smartphone app.

A circular notch in the center of the underlying dressing allows the zipper to stick only to the wound margins and not to the center of the wound so that mechanical contraction forces do not act directly on the central wound tissue.

This “loop adhesion” design is better than traditionally uniform dressing structures, the researchers explain, as it allows the zipper to draw flat against the wound edge—like a drawstring bag—for smoother, more uniform closure.

The device also incorporates a Bluetooth-enabled microcontroller unit, which allows the patient to precisely set and dynamically regulate the wound contraction strength through a mobile app. This intelligent closure system allows contraction to be adjusted according to personal comfort and avoids the pain of over contraction.

Pre-stretched multi-axis wound zippers were better than surgical suturing for linear wounds in rats, achieving immediate and complete closure and a wound healing rate of nearly 90% on the first day.

When used for circular wounds, the wound zipper was also better than surgical suturing and had a superior wound-healing rate above 95% within eight days. It restored the epithelial barrier, reduced the width of the wound, and promoted reconstruction of the collagen matrix.

It was also able to heal the spindle- and oval-shaped wounds frequently seen in the clinic.

Maximum wound closure rates for linear, triangular, rectangular, and circular wounds were 100%, 84.85%, 81.99%, and 87.40%, respectively.

Immunohistochemistry revealed that the wound zipper promoted blood flow to deliver energy and nutrients for healing and supported matrix remodeling to reduce the formation of scar tissue.

Mechanical contraction using the device upregulated vascular regeneration-related transcription factors and speeded the restoration of local perfusion. At the same time, it promoted proliferation and migration of keratinocytes, thereby accelerating re-epithelialization.

In addition, by reducing the skin tension at the wound margin, the wound zipper inhibited the overactivation of myofibroblasts, facilitated orderly collagen matrix remodeling, and decreased the risk of scar formation.

“Collectively, these findings indicate that the MSWZ can deliver rapid, robust, and programmable multi-axis mechanical contraction suited for personalized management of diverse wound types,” the researchers concluded.

“Its conformability to skin and favorable safety profile further support its potential for future clinical translation.”

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STAT+: Private Medicare plans erect barriers to rehab care in pursuit of profit, federal investigators find

The nation’s dominant Medicare Advantage insurers denied rehabilitative care for older and disabled Americans at higher rates than industry peers, then frequently overturned those denials when patients appealed, federal investigators found. The pattern reinforces longstanding concerns that insurers like UnitedHealth Group and Humana are profiting by forcing seriously ill and injured adults 65 and older to fight for care recommended by their doctors.

These health plans hired a UnitedHealth subsidiary called NaviHealth to evaluate requests for rehabilitative care. NaviHealth uses artificial intelligence to examine people’s care needs and was the focus of a STAT investigative series in 2023 that found its denials often resulted in poor outcomes for desperately ill patients.

Now, federal investigators are reporting the insurers themselves concluded NaviHealth’s denials often didn’t stand up to scrutiny. When patients appealed their blocked care, the insurers overturned the company’s denials of nursing home care 97% of the time, according to a report from the Office of Inspector General for the Health and Human Services Department.

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Inclusivity in Insomnia: Adolescents’ Perspectives on the Sleep Solved App: Qualitative Interview Study

Background: Adolescent sleep duration can substantially impact mood, behavior, and academic attainment. While hundreds of sleep-related apps are available to download, none have been cocreated with adolescents from underserved populations in the United Kingdom. Objective: This study aimed to explore adolescents’ views, expectations, and experiences with a novel app to improve sleep, called Sleep Solved, to understand which features were perceived as positive and helpful, and to identify ways to further enhance its usefulness. Sleep Solved is part of a larger stepped behavior change study and was cocreated with adolescents from underserved groups to make the app accessible and engaging for this population. Methods: A total of 63 participants aged 16‐18 years from across the United Kingdom completed semistructured interviews after trying the app. Interviews were analyzed using inductive thematic analysis, as outlined by Braun and Clarke, with a particular focus on the views of individuals from underserved ethnic and socioeconomic groups. Results: Participants perceived Sleep Solved as a useful tool that provides helpful advice regarding changeable behaviors to improve sleep hygiene. Cocreated features of the app, such as the Sleep Stars gamified rewards system and the easy-read, science-based “sleep hacks,” were viewed positively by participants, who reported that they had a beneficial impact on their sleep and sleep schedule. Praise was given for the app’s ease of use and how the science of sleep was explained at an appropriate level, without being overwhelming. Compared to sleep advice on social media platforms, Sleep Solved was considered more reliable and trustworthy. Participants described better sleep hygiene, such as a regular sleep routine and a longer sleep duration, and increased feelings of improved mood and energy. Conclusions: This study found that a cocreated sleep app, designed with input from adolescents in underserved UK populations, was perceived as accessible, reliable, and effective in supporting positive sleep behavior change. Although sleep duration was not objectively tested, participants, particularly those from low socioeconomic status backgrounds and diverse ethnicities, reported improved sleep routines and mood, highlighting the potential of co-designed digital tools to engage and benefit adolescent users.
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GSK to Acquire Nuvalent for $10.6B, Boosting Cancer Pipeline with Precision NSCLC Treatments

GlaxoSmithKline (GSK) has agreed to acquire Nuvalent for $10.6 billion, the companies said, in a deal designed to strengthen the buyer’s cancer pipeline with Nuvalent’s precision oncology treatments—including three non-small cell lung cancer (NSCLC) therapies, of which two are under FDA review with decisions expected later this year.

Boston-based Nuvalent’s pipeline is headed by the ROS1 inhibitor zidesamtinib (NVL-520) and the ALK inhibitor eladalkib (NVL-655), which according to the company represent potential best-in-class, next-generation, highly selective treatments for NSCLC. Both are brain penetrant. The FDA has set target decision dates of September 18 for zidesamtinib and November 27 for neladalkib, both of which have been granted the agency’s Breakthrough Therapy and Orphan Drug designations.

Zidesamtinib is designed to treat NSCLC tumors driven by ROS1 that have developed resistance to currently available ROS1 inhibitors, including tumors with the prevalent G2032R “solvent front” resistance mutation. Zidesamtinib is selective in order to minimize CNS adverse events related to off-target inhibition of the tropomyosin receptor kinase (TRK) family, and potentially drive durable responses for patients with ROS1-mutant variants, Nuvalent says.

Eladalkib was created to address treating tumors driven by ALK that have developed resistance to first-, second-, and third-generation ALK inhibitors, including tumors with both single or compound treatment-emergent ALK mutations such as those involving the G1202R “solvent front” mutation. Eladalkib is also designed to avoiding TRK family inhibition and to treat brain metastases.

The third NSCLC asset of Nuvalent, NVL-330, is a HER2 inhibitor now under study in Phase I trials for HER2-altered NSCLC. In addition, Nuvalent’s pipeline includes an unspecified number of preclinical programs focused on “addressing the limitations of existing therapies for clinically proven kinase targets in oncology,” the company states on its website.

“Today’s acquisition is a multi-product deal, consistent with our approach to acquire assets that have clinically proven targets and meaningfully address an efficacy and/or tolerability gap,” GSK CEO Luke Miels said in a statement. “The two lead products are potential best-in-class assets that could launch this year if approved by the FDA and offer significant new treatment options to patients with two forms of non-small cell lung cancer.”

GSK investors were less enthusiastic as its shares on the London Stock Exchange on Monday dipped 0.5% to 1,903.50 pence. However, Nuvalent shares jumped 39% on Nasdaq to $123.25.

The $10.6 billion Nuvalent acquisition is the third largest merger-and-acquisition (M&A) deal announced this year, behind the €10.7 billion ($12.355 billion) cash buyout offer for Italian-based Recordati being pursued by CVC Capital Partners and Groupe Bruxelles Lambert, which aim to take the company private; and Sun Pharmaceutical Industries’ planned $11.75 billion purchase of Organon, the women’s health drug developer spun out of Merck & Co., in a deal expected to close in early 2027.

Immediate sales opportunities

The Nuvalent candidates, GSK added, present immediate new sales growth opportunities, improving profit contributions from 2027, and a platform in lung cancer for rapid expansion with GSK’s Ris-Rez, a B7-H3 targeted antibody-drug conjugate (ADC) now in Phase III clinical development.

In a presentation to investors after announcing a series of business updates on May 27, Nuvalent projected an ROS1+ NSCLC treatment could generate ~$1.4 billion to $2.1 billion in peak year sales, with about 40% of those sales (from ~$570 million to $855M million) expected to come from the U.S.—multiples above the ~$150 million in peak year sales attained in 2019 by Xalkori® (crizotinib), marketed by Pfizer and Merck KGaA.

An ALK+ NSCLC treatment would potentially be even more lucrative, Nuvalent said last month, with projected worldwide peak year sales ranging from ~$3.4 billion to $5 billion, of which the U.S. would account for 40% of sales, or between ~$1.35 billion and $2 billion—well above the $519 million in peak sales attained in 2023 by Alecensa® (alectinib), marketed by Genentech, a member of the Roche Group and created by Roche-owned Chugai Pharmaceutical.

“Since our founding, we have leveraged our deep expertise in chemistry and structure-based drug design to develop a portfolio of novel, potentially best-in-class kinase inhibitors. Our close collaboration with leading physician-scientists and patient advocates has driven remarkable enrolment, accelerating development and building confidence in the clinical profile of these drugs,” Nuvalent CEO James Porter, PhD, stated. “We’re excited that GSK has recognized the significant value these programs can offer patients and shares our vision for practice-changing innovation.”

Positive pivotal data

In announcing the acquisition, GSK cited positive pivotal data Nuvalent presented at the IASLC 2025 World Conference on Lung Cancer and the 2026 ASCO Annual Meeting. Data at both conferences showed potential best-in-class profiles for zidesamtinib and neladalkib, with both treatments designed to deliver longer effective treatment with better quality of life than current therapies, through high target-selectivity, durable treatment response, improved tolerability, enhanced blood-brain barrier penetration for tumor spread, and broader coverage of ALK and ROS1 mutations.

ROS1- and ALK-altered NSCLC primarily affect non-smoking adults aged 40-50, GSK and Nuvalent said—a patient population the companies described as uniquely defined and engaged.

GSK said it will commence a tender offer to acquire all of Nuvalent’s outstanding shares of Class A and Class B common stock at a purchase price of $124 per share in cash within 10 business days. The expected purchase price represents a 40% premium to the last closing price and a 26% premium to the 30 calendar day volume-weighted average price.

Net of cash acquired, GSK estimated its aggregate investment in Nuvalent to be $9.4 billion.

GSK said the acquisition will not change its 2026 full-year guidance range of 7-9% core operating profit and core EPS growth. The acquisition is expected to contribute to revenue growth from 2027, be incremental to GSK’s existing ambition for sales of >£40 billion (>$53.56 billion) by 2031, and strengthen the company’s core operating profit through the two-year period of loss of exclusivity for its aging blockbuster dolutegravir (2028-2030).

Dolutegravir is an HIV-1 integrase strand transfer inhibitor (INSTI) marketed as the monotherapy Tivicay® by Viiv Healthcare, in which GSK holds a 78.3% majority stake (and Shionogi, the remaining 21.7% after Pfizer cashed out its 11.7% stake, receiving $1.88 billion). Dolutegravir is also included in Viiv’s fixed-dose HIV combination therapies Dovato (dolutegravir and lamivudine) and Juluca (dolutegravir and rilpivirine).

Adding to core profit, EPS

GSK said it expected to add to its core operating profit in 2027 and core earnings per share (EPS) in 2029 by acquiring Nuvalent, even after accounting for cost-cutting synergies and “reprioritization,” which it defines as the shifting of personnel, capital, and other resources away from lower-yield, early-stage research or legacy programs toward higher-value clinical assets and corporate activities. Nuvalent reported 228 full-time employees, of which 144 are engaged in R&D, in its Form 10-K annual report for 2025, filed February 26.

Should the transaction close in Q3 2026 as expected, GSK said it expects low single-digit percentage dilution to core EPS this year through 2028.

The company said it will fund the Nuvalent acquisition primarily from new and existing debt facilities plus cash, with no impact expected to its credit rating. GSK ended Q1 with £3.442 billion ($4.608 billion) in cash and cash equivalents, up 1.3% from £3.397 billion ($4.548 billion) at the end of 2025.

The transaction is subject to customary closing conditions, including the tender of a majority of Nuvalent’s outstanding shares of Class A common stock in the tender offer and the expiration or termination of the applicable waiting period under the Hart-Scott-Rodino Act in the U.S. Soon after the closing of the tender offer, GSK expects to acquire any remaining shares of Nuvalent through a second-step merger under Delaware law at the same price per share.

GSK said it will account for the transaction as a business combination and assume Nuvalent’s existing revenue-sharing arrangements of low-single-digit royalties payable to Royalty Pharma and Deerfield. Royalty Pharma in December acquired for up to $315 million a pre-existing royalty interest in zidesamtinib and neladalkib from an undisclosed third party. Deerfield is Nuvalent’s largest shareholder.

“GSK’s proven track record, infrastructure, and expertise will support the successful commercialization of zidesamtinib and neladalkib, as well as accelerate advancement of our broader discovery pipeline,” Porter added.

The post GSK to Acquire Nuvalent for $10.6B, Boosting Cancer Pipeline with Precision NSCLC Treatments appeared first on GEN – Genetic Engineering and Biotechnology News.

Origins of First Eukaryotes Linked to Contributions from Multiple Bacteria and Giant Viruses

All cells in animals, plants, fungi, and protists share a fundamental characteristic, in that they are eukaryotic cells. These are essentially complex cells with specialized internal compartments. The cells that make up our bodies are no exception.

How this type of cell emerged is one of the great questions in biology. For decades, the dominant explanation has placed acquisition of the mitochondrion as the ultimate turning point. It’s thought that an archaeon established a symbiotic relationship with a bacterium, which eventually became the mitochondrion, and this alliance opened the door to cellular complexity.

A study led by Toni Gabaldón, PhD, an ICREA researcher at IRB Barcelona and the Barcelona Supercomputing Center-Centro Nacional de Supercomputación (BSC-CNS) now rethinks this view. While the research does not deny the central role of the mitochondrion, it suggests that the origin of complex cells was a longer, more gradual and more collaborative process than had previously been thought. Challenging the idea that cellular complexity emerged from a single evolutionary encounter, the study results point instead to a gradual process of interactions among different microorganisms that lasted for millions of years. The findings identify contributions from several bacteria, in addition to the one that gave rise to the mitochondria, and suggest that giant viruses may have acted as vehicles for genetic transfer.

“For a long time, we have explained the origin of complex cells as a story with two main protagonists: an archaeon and the bacterium that gave rise to the mitochondrion,” said Gabaldón. “Our study suggests that this narrative is incomplete and that there were more actors on stage, including other bacterial groups and giant viruses that may have facilitated gene exchange.” The team published their findings in Nature, in a paper titled “Gene ancestries reveal diverse microbial associations during eukaryogenesis.”

“The origin of eukaryotes remains a central enigma in biology,” the authors wrote. Unlike studies with dinosaurs, the origin of eukaryotes cannot be reconstructed from visible bones or fossils. It likely occurred about two billion years ago in microscopic organisms, of which barely any direct traces remain. “The current consensus on eukaryogenesis revolves around scenarios that always involve an endosymbiotic relationship with extensive gene transfer between an alphaproteobacterial endosymbiont and a host with an Asgard archaeal ancestry,” the team noted. However, the footprints of this evolution are still present in today’s genomes.

To trace them, the team approached the problem as a form of computational molecular archaeology, using the computing power of the MareNostrum series of supercomputers to analyze public genomic data spanning biodiversity as a whole.

The researchers first reconstructed the repertoire of gene and protein families of the last common ancestor of all eukaryotes, known as LECA (last eukaryotic common ancestor). “Our analysis provided a revised reconstruction of the last eukaryotic common ancestor (LECA) proteome, in which we traced the phylogenetic origin of each protein family,” they wrote. The investigators then analyzed its evolutionary origin by comparing these families against databases containing tens of thousands of bacterial, archaeal, and viral genomes.

“We are trying to reconstruct a story that took place billions of years ago and for which we have no direct fossils. That is why we have been very conservative: we only kept the most robust evolutionary signals—those with a strength comparable to the signals already accepted for the ancestral archaeon and for the bacterium that gave rise to the mitochondrion,” explain study co-authors Moisès Bernabeu, PhD, Saioa Manzano-Morales, PhD, and Marina Marcet-Houben, PhD, who are researchers in the Comparative Genomics group led by Gabaldón at IRB Barcelona and the BSC.

After more than five years of work using complex mathematical models and processing large volumes of genomic sequences, the team was able to detect signals that would otherwise have remained invisible.

Beyond the mitochondrion, the study identifies two particularly relevant bacterial signals: Myxococcota and Planctomycetota. The former are related to metabolic functions, including processes linked to lipids and membranes. The latter are bacteria known for their structural complexity, featuring internal compartments that are unusual for bacterial organisms. “Transfers from these donors have been identified in earlier studies, including small-scale detailed ones such as the acquisition of some steroid biosynthesis enzymes from Myxococcota,” the team stated.

Their analyses indicate that these contributions did not happen all at once. Planctomycetota appear as an older signal, whereas Myxococcota and the bacterium that gave rise to the mitochondrion show signals that are closer in time. “We found compelling evidence for multiple waves of horizontal gene transfer from diverse bacterial donors, with some likely to have preceded mitochondrial endosymbiosis,” the scientists suggested.

One of the most unexpected findings of the study is that some genes integrated during the early evolution of eukaryotes appear to come from giant viruses, specifically Nucleocytoviricota. These viruses have genomes that are much larger than those of most known viruses, and they infect single-celled eukaryotic organisms.

The authors propose that these viruses could have acted as vehicles for genetic transfer between microorganisms coexisting in the same ecosystem, facilitating exchanges that helped shape the ancestral genome of eukaryotic cells. “Our results confirm and expand earlier results supporting sizeable gene flow from diverse prokaryotic ancestors preceding the LECA4, and uncover a role for viruses as potential mediators of such transfers,” the scientists stated.

This vision fits with the idea that the ancestors of eukaryotic cells lived in environments rich in microbial communities, such as microbial mats, where different microorganisms coexist in layers under varying chemical conditions. In this context, genetic exchanges would have allowed them to acquire new biological capabilities over time. “Microorganisms are known to form complex communities such as microbial mats or complex biofilms, of which viruses also form active part, and it is reasonable to consider that the ancestors of the LECA lived in such complex environments,” they stated.

The study addresses one of the major questions in biology: how the complexity of the cells that form our bodies came to be. By reconstructing the genetic traces of that process, the work provides a new perspective on a key episode in the history of life: the origin of the cellular lineage to which animals, plants, fungi, and protists belong. “Taken together, our results suggest that ancient eukaryotes may have originated within complex microbial ecosystems through a succession of diverse associations that left a footprint of horizontally transferred genes.”

The paper expands on a line of research initiated by Gabaldón in 2016, when he published a study in Nature that already suggested the mitochondrion might have been acquired relatively late in the process of eukaryotic origins. Now, with much more genomic data available and more powerful computational tools, the team has been able to analyze in greater detail which other organisms left their mark on that common ancestor.

“All genomes preserve traces of their history. In the case of eukaryotes, those traces tell us of ancient alliances between microorganisms. Understanding them helps us answer a very profound question: what we are and where we come from,” commented Gabaldón.

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Diabetes association leader apologizes for expulsion of members, pledges to rebuild trust

Five days after five members of the American Diabetes Association were ushered out of its annual scientific sessions in New Orleans for handing out an editorial criticizing federal research cuts, ADA chief executive officer Charles Henderson on Wednesday apologized to the people expelled and to the broader diabetes community.

“First and foremost, I want to personally apologize to Dr. Steven Kahn, Dr. Desmond Schatz, Dr. Aaron Kelly, Dr. Maureen Gannon, and Dr. Justin Ryder, who were escorted out and denied access to scientific sessions, regardless of the circumstances that led to those events,” Henderson said in the three-minute video. “I recognize the impact that experience had on each of you. I am deeply sorry for the hurt, frustration, and the pain that resulted.”

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Brain Aneurysm Study Identifies Structural, Immune Markers of Rupture Risk

According to some estimates, stroke is the second leading cause of death globally. One of the causes of a severe type of stroke are brain aneurysms. Now data from a new study suggests that certain cells in the brain may cause aneurysms to weaken and rupture. And it helps explain why some aneurysms burst while others do not. It also opens a door to new ways of potentially predicting and preventing strokes. All of the findings are covered in a new Nature Neuroscience paper titled “Cerebrovascular vulnerability and fibrosis in human brain aneurysms.”

Brain aneurysms, which are bulges in blood vessels in the brain, can go unnoticed for years before rupturing causing a severe, often deadly type of stroke. About one in 50 people in the U.S. has a brain aneurysm but predicting which ones are most dangerous remains challenging. Aneurysms can be repaired surgically or using other minimally invasive procedures but those decisions depend on the size and location of the aneurysm as well as patient specific risk factors. With the current study, “we’ve made major steps toward solving the mystery of how aneurysms form,” said Ethan Winkler, MD, PhD, assistant professor of neurological surgeon and senior author of the Nature Neuroscience study. “We’ve identified the cast of characters involved and seen which ones are implicated at different phases of disease.”

To get to those answers, Winkler and his team analyzed more than 100,000 individual cells from human aneurysms and healthy brain arteries. From these data, they identified 19 transcriptionally distinct cell types and determined which genes were active in each. They also mapped how the cells were organized within the blood vessel wall.

“Our atlas of human brain aneurysms, as well as cell-resolution spatial transcriptomics, revealed that pathological cerebrovascular remodeling occurs with the loss of structurally supportive smooth muscle cells and the emergence of activated perivascular fibroblasts, which re-populate the vascular wall and express multiple genes linked to aneurysm risk,” the scientists wrote. 

Specifically, they found that vessels in aneurysm tissue had disorganized layers, and that many of the smooth muscle cells that allows the vessel walls to expand and contract had disappeared. In their place were scar-forming fibroblasts, which the team dubbed “activated fibroblasts.” These stiffened the arterial wall, making it less able to flex as blood flowed through. These cells also expressed genes that are linked to an inherited risk of aneurysm. The scientists also identified a type of macrophage that accumulated inside the arterial wall near the fibroblasts. The data showed that these specialized macrophages express a gene that is typically associated with bone tissue. 

Further testing revealed the presence of a feedback look between the two cell types. Specifically, the activated fibroblasts release a signal that triggers the macrophages to produce enzymes that degrade the blood vessel’s structural support. The scientists confirmed that this was the case by blocking the signals sent to the macrophages. They observed that the macrophages were less likely to produce the destructive enzymes when the signal was blocked. 

This process where vessel walls lose muscle cells followed by the buildup of scar tissue and immune cell activation helps explain why smaller aneurysms, which are often considered low risk, can still rupture. It jibes with Winkler’s own clinical experiences. He noted that more than half of the ruptures that he treated early in his career occurred in aneurysms below the typical surgical threshold of seven millimeters.  

This study brings scientists and clinicians one step closer to understanding how aneurysms form and perhaps being able to intervene earlier to prevent them. As the scientists note in the paper, “the molecular blueprint provided by this study substantially extends our mechanistic understanding of brain aneurysms and nominates new cells and pathways with translational promise for the development of therapeutic options.” This could involve blocking the signals that fibroblasts send or by inhibiting the immune response to those signals.               

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