Communications medicine最新文献

{"title":"A nationwide study of risk factors for long COVID and its economic and mental health consequences in the United States.","authors":"Daniel Kim","doi":"10.1038/s43856-025-00759-0","DOIUrl":"https://doi.org/10.1038/s43856-025-00759-0","url":null,"abstract":"<p><strong>Background: </strong>In the United States, concerns have been increasingly raised over the future public health and economic burden of long COVID including disability and declines in labor force participation. However, only a handful of U.S. studies have explored sociodemographic or socioeconomic characteristics that put people at risk of long COVID or have investigated its economic and mental health sequelae.</p><p><strong>Methods: </strong>Using repeated cross-sectional data on over 375,000 adults including nearly 50,000 adults with long COVID pooled from U.S. nationally-representative Household Pulse Survey data collected between September and November 2022 and between August and October 2023, I fit age- and gender-adjusted and multivariable modified Poisson regression models to examine multiple sociodemographic and socioeconomic factors as predictors of long COVID. I further estimate the risks of unemployment, financial hardship, and anxiety and depression among working-aged adults and adults with current long COVID symptoms, and estimate the economic burden of lost wages due to long COVID.</p><p><strong>Results: </strong>Nearly one in seven adults (~35 million) and working-aged adults (~30 million) reported having a history of long COVID by late 2022 and late 2023. In age- and gender-adjusted models and fully-adjusted multivariable models, I find several factors predict long COVID including lower household income, and being Hispanic, female, gay/lesbian or bisexual. I also find having long COVID is linked to higher risks of recent unemployment, financial hardship, and anxiety and depressive symptomatology, with evidence of dose-response relationships.</p><p><strong>Conclusions: </strong>Overall, an estimated 24 million working-aged adults with long COVID had been or may still be at risk of adverse socioeconomic and mental health outcomes. The lost earnings due to long COVID among working-aged adults are estimated to total $211 billion in 2022 and $218 billion in 2023. These findings highlight the substantial public health and economic implications of long COVID among Americans.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"104"},"PeriodicalIF":5.4,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143813179","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2 dynamics in New York City during March 2020-August 2023.","authors":"Wan Yang, Hilary Parton, Wenhui Li, Elizabeth A Watts, Ellen Lee, Haokun Yuan","doi":"10.1038/s43856-025-00826-6","DOIUrl":"10.1038/s43856-025-00826-6","url":null,"abstract":"<p><strong>Background: </strong>The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has been widespread since 2020 and will likely continue to cause substantial recurring epidemics. However, understanding the underlying infection burden and dynamics, particularly since late 2021 when the Omicron variant emerged, is challenging. Here, we leverage extensive surveillance data available in New York City (NYC) and a comprehensive model-inference system to reconstruct SARS-CoV-2 dynamics therein through August 2023.</p><p><strong>Methods: </strong>We fit a metapopulation network SEIRSV (Susceptible-Exposed-Infectious-(re)Susceptible-Vaccination) model to age- and neighborhood-specific data of COVID-19 cases, emergency department visits, and deaths in NYC from the pandemic onset in March 2020 to August 2023. We further validate the model-inference estimates using independent SARS-CoV-2 wastewater viral load data.</p><p><strong>Results: </strong>The validated model-inference estimates indicate a very high infection burden-the number of infections (i.e., including undetected asymptomatic/mild infections) totaled twice the population size ( > 5 times documented case count) during the first 3.5 years. Estimated virus transmissibility increased around 3-fold, whereas estimated infection-fatality risk (IFR) decreased by >10-fold during this period. The detailed estimates also reveal highly complex variant dynamics and immune landscape, and higher infection risk during winter in NYC over the study period.</p><p><strong>Conclusions: </strong>This study provides highly detailed epidemiological estimates and identifies key transmission dynamics and drivers of SARS-CoV-2 during its first 3.5 years of circulation in a large urban center (i.e., NYC). These transmission dynamics and drivers may be relevant to other populations and inform future planning to help mitigate the public health burden of SARS-CoV-2.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"102"},"PeriodicalIF":5.4,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143805042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mini-GRID therapy delivers optimised spatially fractionated radiation therapy using a flattening free filter accelerator.","authors":"M Isabel Acuña, Charlotte Lamirault, Thibaut Larcher, Elise Brisebard, Tim Schneider, Marjorie Juchaux, Ramon Iglesias-Rey, Sabela Fernández-Rodicio, Pablo Aguiar, Noemi Gómez-Lado, Immaculada Martínez-Rovira, Roberto González-Vegas, Ibraheem Yousef, Antonio Gomez-Caamano, Miguel Pombar, Victor Luna, Manuel Sanchez, Yolanda Prezado","doi":"10.1038/s43856-025-00809-7","DOIUrl":"10.1038/s43856-025-00809-7","url":null,"abstract":"<p><strong>Background: </strong>Radioresistant tumours remain a challenge for conventional radiation therapy (RT), and often, only palliative treatment can be offered. Recently developed techniques, such as spatially fractionated radiation therapy (SFRT) could potentially improve treatment. However, current clinical SFRT implementations do not allow the full potential to be exploited. We further optimize SFRT, developing mini-GRID, which uses a flattening free filter accelerator.</p><p><strong>Methods: </strong>The increase in normal tissue tolerances provided by mini-GRID compared to conventional RT and GRID therapy was validated in a rat model of brain irradiation in a longitudinal imaging study, behavioural tests and by histopathological evaluation.</p><p><strong>Results: </strong>The implementation optimizes mini-GRID therapy, with beam widths around 2 mm². The peak-to-valley dose ratios and peak dose rates are around 4 and 7 Gy/min, respectively. Mini-GRID RT allows the use of high peak doses: 42 Gy in one fraction, a factor more than twice higher than the peak doses generally employed in conventional GRID therapy (20 Gy peak dose). This enables the use of more aggressive and potentially curative treatments. Infrared microspectroscopy analysis suggests different early biochemical changes in both modalities, with conventional RT leading to stronger modifications in the secondary protein structure, and higher oxidative damage than mini-GRID RT.</p><p><strong>Conclusions: </strong>The possibility to treat both large and small tumours, and to perform safe and potentially curative dose escalations in previously untreatable cases, makes mini-GRID a promising approach to expand the clinical use of SFRT.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"101"},"PeriodicalIF":5.4,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972377/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143789492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Keratinocyte SR-B1 expression and targeting in cytokine-driven skin inflammation.","authors":"Jacquelyn Trujillo, Andrea E Calvert, Jonathan S Rink, Bethany E Perez White, Fabiola Sepulveda, Dauren Biyashev, Kurt Q Lu, Robert M Lavker, Han Peng, C Shad Thaxton","doi":"10.1038/s43856-025-00804-y","DOIUrl":"10.1038/s43856-025-00804-y","url":null,"abstract":"<p><strong>Background: </strong>Strategies to treat inflammatory skin conditions require identifying new targets involved in interactions between overlying epithelial and underlying dermal immune cells. Scavenger receptor class B type 1 (SR-B1) is a cell surface receptor that binds high-density lipoproteins (HDL) and mediates inflammatory responses in immune and endothelial cells. The SR-B1 receptor is also expressed in keratinocytes, but its role in inflammatory skin diseases remains unexplored.</p><p><strong>Methods: </strong>To investigate keratinocyte SR-B1 in the setting of inflammation, we measured its expression in skin biopsy samples obtained from patients with psoriasis; human skin explants exposed to the inflammatory cytokine, interleukin-17A (IL-17A); and mouse skin exposed to the pro-inflammatory agent, imiquimod (IMQ). We also evaluated the effects of SR-B1 knockdown on primary keratinocyte responses to IL-17A. Finally, we employed a synthetic HDL-nanoparticle (HDL NP) to investigate the therapeutic potential of targeting SR-B1 in IL-17A-stimulated keratinocytes and in male C57BL/6 mice with IMQ-induced skin inflammation.</p><p><strong>Results: </strong>Our data show SR-B1 expression is increased in diseased human skin and in both human and mouse models of skin inflammation. SR-B1 knockdown in keratinocytes exacerbates the inflammatory response to IL-17A, whereas targeting SR-B1 with HDL NP attenuates this response. In the IMQ murine model, topical application of HDL NPs improves the skin phenotype, normalizes SR-B1 expression, and reduces molecular and cellular markers of inflammation.</p><p><strong>Conclusions: </strong>Overall, SR-B1 plays a role in skin inflammation and HDL NP-mediated targeting of SR-B1 in keratinocytes may offer a targeted new therapy for inflammatory skin disease.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"100"},"PeriodicalIF":5.4,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11968926/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functionally enriched epigenetic clocks reveal tissue-specific discordant aging patterns in individuals with cancer.","authors":"Chiara M S Herzog, Elisa Redl, James Barrett, Sepideh Aminzadeh-Gohari, Daniela D Weber, Julia Tevini, Roland Lang, Barbara Kofler, Martin Widschwendter","doi":"10.1038/s43856-025-00739-4","DOIUrl":"10.1038/s43856-025-00739-4","url":null,"abstract":"<p><strong>Background: </strong>Aging is a key risk factor for many diseases, including cancer, and a better understanding of its underlying molecular mechanisms may help to prevent, delay, or treat age-related pathologies. Epigenetic alterations such as DNA methylation (DNAme) changes are a hallmark of aging and form the basis of so-called epigenetic clocks, yet their functional relevance and directionality in different organs during disease development is often unclear.</p><p><strong>Methods: </strong>Here, we link cell-specific age-related DNAme changes with three key hallmarks of aging and cancer (senescence, promoter methylation in genes associated with stem cell fate, and dysregulated proliferation) to comprehensively dissect their association with current and future cancer development, carcinogen exposure or preventive measures, and mortality using data in different organs from over 12,510 human and 105 mouse samples, benchmarking against existing epigenetic clocks.</p><p><strong>Results: </strong>Our findings offer insights into the association of functionally enriched groups of age-related DNAme changes with cancer, identify sites perturbed earliest during carcinogenesis, as well as those distinct between cancer and reprogramming that could inform strategies to prevent teratoma formation upon in vivo reprogramming. Surprisingly, both mouse and human data reveal accelerated aging in breast cancer tissue but decelerated epigenetic aging in some non-cancer surrogate samples from breast cancer patients, in particular cervical samples.</p><p><strong>Conclusions: </strong>This work provides evidence for discordant systemic tissue aging in breast cancer.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"98"},"PeriodicalIF":5.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic signatures in surrogate tissues are able to assess cancer risk and indicate the efficacy of preventive measures.","authors":"James E Barrett, Chiara Maria Herzog, Sepideh Aminzadeh-Gohari, Elisa Redl, Isma Ishaq Parveen, Julia Rothärmel, Julia Tevini, Daniela D Weber, Luca Catalano, Victoria E Stefan, Thomas K Felder, Peter Obrist, Twana Alkasalias, Kristina Gemzell-Danielsson, Roland Lang, Barbara Kofler, Martin Widschwendter","doi":"10.1038/s43856-025-00779-w","DOIUrl":"10.1038/s43856-025-00779-w","url":null,"abstract":"<p><strong>Background: </strong>In order to advance personalized primary cancer prevention, surrogate endpoint biomarkers in distant, easy to access tissues (i.e., field defect indicators) reflecting field cancerization in the organ at risk are essential.</p><p><strong>Methods: </strong>Here we utilized medroxyprogesterone acetate and 7,12-dimethylbenzanthracene to induce mammary gland cancers in mice. We assessed epigenetic signatures reflective of carcinogen exposure, cell-type composition, mitotic age, and methylation at progesterone receptor binding sites in both, the tissue at risk (normal mammary gland; field cancerization) and distant non-at-risk organs (cervix, oviduct, and blood; field defect indicators), in mice that did and did not develop mammary gland cancers.</p><p><strong>Results: </strong>We demonstrate that the anti-progestine mifepristone reduces the cancer risk by more than 50%. Importantly, the reduction in cancer risk is accompanied by a decline in both field cancerization and field defect indicators; specifically, epigenetic signatures in the cervix are predictive of mammary cancer formation but show tissue-specific directionality.</p><p><strong>Conclusions: </strong>These data encourage further exploration of epigenetic biomarkers in certain field defect-indicating tissues with a view to monitor the efficacy of cancer prevention strategies in humans.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"97"},"PeriodicalIF":5.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11965489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Call for a fairer approach to authorship in publishing biomedical research.","authors":"Phaik Yeong Cheah, Michael Parker","doi":"10.1038/s43856-025-00815-9","DOIUrl":"10.1038/s43856-025-00815-9","url":null,"abstract":"<p><p>In this Perspective article, we call for a fairer approach to authorship practice in collaborative biomedical research to promote equity and inclusiveness. Current practice does not adequately recognise all contributors involved in different stages of the work and may exacerbate preexisting inequalities. Here, we discuss some key features of contemporary collaborative research practice that complicate authorship decisions. These include the project size, complexity of multidisciplinary team involvement and researchers having varying degrees of expertise and experience. We conclude by making some suggestions to address these concerns.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"99"},"PeriodicalIF":5.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11961711/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143766001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive testing of large language models for extraction of structured data in pathology.","authors":"Bastian Grothey, Jan Odenkirchen, Adnan Brkic, Birgid Schömig-Markiefka, Alexander Quaas, Reinhard Büttner, Yuri Tolkach","doi":"10.1038/s43856-025-00808-8","DOIUrl":"10.1038/s43856-025-00808-8","url":null,"abstract":"<p><strong>Background: </strong>Pathology departments generate large volumes of unstructured data as free-text diagnostic reports. Converting these reports into structured formats for analytics or artificial intelligence projects requires substantial manual effort by specialized personnel. While recent studies show promise in using advanced language models for structuring pathology data, they primarily rely on proprietary models, raising cost and privacy concerns. Additionally, important aspects such as prompt engineering and model quantization for deployment on consumer-grade hardware remain unaddressed.</p><p><strong>Methods: </strong>We created a dataset of 579 annotated pathology reports in German and English versions. Six language models (proprietary: GPT-4; open-source: Llama2 13B, Llama2 70B, Llama3 8B, Llama3 70B, and Qwen2.5 7B) were evaluated for their ability to extract eleven key parameters from these reports. Additionally, we investigated model performance across different prompt engineering strategies and model quantization techniques to assess practical deployment scenarios.</p><p><strong>Results: </strong>Here we show that open-source language models extract structured data from pathology reports with high precision, matching the accuracy of proprietary GPT-4 model. The precision varies significantly across different models and configurations. These variations depend on specific prompt engineering strategies and quantization methods used during model deployment.</p><p><strong>Conclusions: </strong>Open-source language models demonstrate comparable performance to proprietary solutions in structuring pathology report data. This finding has significant implications for healthcare institutions seeking cost-effective, privacy-preserving data structuring solutions. The variations in model performance across different configurations provide valuable insights for practical deployment in pathology departments. Our publicly available bilingual dataset serves as both a benchmark and a resource for future research.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"96"},"PeriodicalIF":5.4,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11958830/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756258","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preclinical extracellular matrix-based treatment strategies for myocardial infarction: a systematic review and meta-analysis.","authors":"Atze van der Pol, Marijn C Peters, Ignasi Jorba, Anke M Smits, Niels P van der Kaaij, Marie-Jose Goumans, Kimberley E Wever, Carlijn V C Bouten","doi":"10.1038/s43856-025-00812-y","DOIUrl":"10.1038/s43856-025-00812-y","url":null,"abstract":"<p><strong>Background: </strong>Administrating extracellular matrix (ECM) to restore cardiac function post-myocardial infarction (MI) shows promise, however study variability obscures its true impact. We therefore conducted a systematic review and meta-analysis of preclinical studies to assess the effects of ECM treatments on cardiac function and tissue homeostasis post-MI.</p><p><strong>Methods: </strong>We searched PubMed and SCOPUS from inception to June 28, 2024, for animal studies describing ECM treatment post-MI (pre-registered on PROSPERO, CRD42022368400). Random effects meta-analyses compared ECM treatment to controls regarding left ventricular ejection fraction (LVEF), fractional shortening, infarct size, stroke volume, and left ventricular wall thickness. Subgroup analyses examined the influence of sex, species, ECM source, and administration method. Funnel plots and Egger's regression assessed publication bias.</p><p><strong>Results: </strong>We identify 88 articles which meet our inclusion criteria. These studies describe the use of rats (51%), mice (38%), and pigs (11%). 44% of studies use males, 34% females, 5% both sexes, and 17% did not report sex. Most studies employ permanent MI models (85%) over ischemia reperfusion models (15%), and deliver ECM via intramyocardial injection (59%), cardiac patch (39%), cardiac sleeve (1%), or osmotic pump (1%). Our meta-analysis demonstrates that ECM treatment significantly improves LVEF (MD: 10.9%, 95% CI: [8.7%;13.0%]; p = 8.057e-24), fractional shortening (MD: 8.2%, 95% CI: [5.6%; 10.9%]; p = 1.751e-09), stroke volume (SMD 0.6, 95% CI: [0.2;1.0], p = 0.004), left ventricular wall thickening (SMD 1.2, 95% CI: [0.9; 1.5], p = 1.321e-17), while reducing infarct size (-11.7%, 95% CI: [-14.7%;-8.6%], p = 3.699e-14). We find no significant differences between the various subgroups and no indication of publication bias.</p><p><strong>Conclusions: </strong>ECM-based treatments significantly enhance cardiac function and tissue homeostasis in preclinical post-MI models, supporting further research toward clinical translation.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"95"},"PeriodicalIF":5.4,"publicationDate":"2025-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11955565/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143756260","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Real-world impact of physical activity reward-driven digital app use on cardiometabolic and cardiovascular disease incidence.","authors":"Adi Berliner Senderey, Tom Mushkat, Ofer Hadass, Daphna Carmeli, Samah Hayek, Marie-Laura Charpingnon, Eyal Jacobson, Ran D Balicer","doi":"10.1038/s43856-025-00792-z","DOIUrl":"10.1038/s43856-025-00792-z","url":null,"abstract":"<p><strong>Background: </strong>The lack of effective tools available to health providers for enhancing patient physical activity prompts this study to examine the real-world impact of a physical activity reward-driven app on health outcomes, utilizing Electronic Health Records (EHR) data from Israel's largest healthcare organization.</p><p><strong>Methods: </strong>Conducting a retrospective cohort study, we matched app-users to non-users based on demographic and clinical characteristics.</p><p><strong>Results: </strong>App-users have a significantly lower risk of cardiovascular disease (HR 0.95), stroke (HR 0.91), and type 2 diabetes (HR 0.82) compared to non-app users. Higher levels of physical activity among app users further reduce the incidence of cardiovascular disease (HR 0.87), stroke (HR 0.84), and type 2 diabetes (HR 0.75) compared with non-app user. However, engagement in mild physical activity, as measured by step count, does not differ from non- users in the incidence of these conditions.</p><p><strong>Conclusions: </strong>These findings highlight the potential of app-based interventions to promote higher levels of physical activity and mitigate major vascular and metabolic illnesses.</p>","PeriodicalId":72646,"journal":{"name":"Communications medicine","volume":"5 1","pages":"94"},"PeriodicalIF":5.4,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11950345/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143733478","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}