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ObjectiveComprehensive data and analyses on cardiovascular research could clarify recent research trends for the academic community and facilitate policy development. We examined publications and reference data to identify research topics, trends and interdisciplinarity for cardiovascular disease (CVD).MethodsWe extracted and clustered text fragments from the titles and abstracts of 2 512 445 publications using artificial intelligence techniques, including natural language processing (NLP) for semantic analysis. Cardiovascular experts identified topics and document clusters based on the output of those semiautomatic methods. We also applied machine learning algorithms to predict the trends over the next 5 years in each field. We examined the crossover between the two cluster groups using citation relationships in the documents.ResultsResearch in clinical studies showed the most notable increase; that was followed by research in population and basic studies. The research hotspots were minimally invasive treatments for valve disease, circulatory haemodynamics, and prevention and control of hypertension. The fastest-growing topics were health monitoring, evidence-based medicine and immunotherapy. We found extensive crossover relationships among document clusters for the periods of 2017–2018 and 2020–2021.ConclusionsThis study provides valuable insights into the research hotspots for cardiovascular research, including an increasing emphasis on early disease detection and prevention, exploration of minimally invasive treatments and assessment of risk factors. The research landscape demonstrates signs of interdisciplinarity and integration as reflected in citation relationships. These findings suggest practical implications for optimising resource allocation in healthcare systems, guiding clinical guideline updates and informing policy-making to prioritise high-impact research areas aligned with evolving CVD challenges. Given the evolving global burden of CVD, continuous research and innovation are imperative, with interdisciplinary collaboration assuming a pivotal role in advancing scientific knowledge.

Recent single-arm studies involving neoadjuvant camrelizumab, a PD-1 inhibitor, plus chemotherapy for resectable locally advanced esophageal squamous cell carcinoma (LA-ESCC) have shown promising results. This multicenter, randomized, open-label phase 3 trial aimed to further assess the efficacy and safety of neoadjuvant camrelizumab plus chemotherapy followed by adjuvant camrelizumab, compared to neoadjuvant chemotherapy alone. A total of 391 patients with resectable thoracic LA-ESCC (T1b-3N1-3M0 or T3N0M0) were stratified by clinical stage (I/II, III or IVA) and randomized in a 1:1:1 ratio to undergo two cycles of neoadjuvant therapy. Treatments included camrelizumab, albumin-bound paclitaxel and cisplatin (Cam+nab-TP group; n  = 132); camrelizumab, paclitaxel and cisplatin (Cam+TP group; n  = 130); and paclitaxel with cisplatin (TP group; n  = 129), followed by surgical resection. Both the Cam+nab-TP and Cam+TP groups also received adjuvant camrelizumab. The dual primary endpoints were the rate of pathological complete response (pCR), as evaluated by a blind independent review committee, and event-free survival (EFS), as assessed by investigators. This study reports the final analysis of pCR rates. In the intention-to-treat population, the Cam+nab-TP and Cam+TP groups exhibited significantly higher pCR rates of 28.0% and 15.4%, respectively, compared to 4.7% in the TP group (Cam+nab-TP versus TP: difference 23.5%, 95% confidence interval (CI) 15.1–32.0, P  < 0.0001; Cam+TP versus TP: difference 10.9%, 95% CI 3.7–18.1, P  = 0.0034). The study met its primary endpoint of pCR; however, EFS is not yet mature. The incidence of grade ≥3 treatment-related adverse events during neoadjuvant treatment was 34.1% for the Cam+nab-TP group, 29.2% for the Cam+TP group and 28.8% for the TP group; the postoperative complication rates were 34.2%, 38.8% and 32.0%, respectively. Neoadjuvant camrelizumab plus chemotherapy demonstrated superior pCR rates compared to chemotherapy alone for LA-ESCC, with a tolerable safety profile. Chinese Clinical Trial Registry identifier: ChiCTR2000040034 . In a randomized phase 3 trial, neoadjuvant anti-PD-1 plus either paclitaxel and cisplatin or nab-paclitaxel and cisplatin elicited a significantly superior pathological complete response rate versus neoadjuvant paclitaxel and cisplatin alone in patients with resectable locally advanced esophageal squamous cell carcinoma.

Esophageal carcinoma (EC) is a tremendous threat to human health and life worldwide. Long non-coding RNAs (lncRNAs) have been identified as crucial players in carcinomas including EC. An in-depth understanding on regulatory networks of lncRNAs contributes to the better management of EC. In this text, 2052 lncRNAs and 3240 mRNAs were found to be differentially expressed in 5 EC tumor tissues versus adjacent normal tissues by microarray analysis. Moreover, 297 carcinoma-related genes were screened out according to pathway and disease annotation analyses. In addition, 410 potential lncRNA-mRNA cis-regulation pairs and 395 lncRNA-mRNA trans-regulation pairs were screened out. Among these genes, 14 trans-regulated and 19 cis-regulated genes were found to be related with carcinomas. Additionally, 42 possible lncRNA-mRNA trans-regulation pairs and 26 cis-regulation pairs were found to be related with carcinomas. Also, 4 differentially expressed transcription factors in EC and lncRNAs possibly regulated by these transcription factors were screened out. Moreover, plenty of common upregulated or downregulated lncRNAs and mRNAs in EC were identified by comparative analysis for our microarray outcomes and previous high-throughput data. Furthermore, we demonstrated that ENST00000437781.1 knockdown inhibited cell proliferation and facilitated cell apoptosis by downregulating SIX homeobox 4 (SIX4) and ENST00000524987.1 knockdown had no influence on anoctamin 1 calcium activated chloride channel (ANO1) expression in EC cells. In conclusion, we identified some crucial lncRNAs and genes along with potential regulatory networks of lncRNAs/genes, deepening our understanding on pathogenesis of EC.

Lumbar intervertebral disc degeneration, a key indicator of aging in the human movement system, is linked to increasing global cases of low back pain. Current diagnostic methods rely on imaging and physician experience, lacking predictive tools and personalized treatment strategies. This study used a multicenter lumbar MRI dataset to map disc degeneration in the Chinese population, revealing three accelerated degeneration phases during the lifecycle. Age heatmaps highlighted the degeneration rate of L1-L3 segments, highly synchronized with true age, serving as a baseline for physiological aging estimation. A contrastive learning-based slice ensemble network achieved a mean absolute error of 2.59 years in age estimation, and multi-center validation confirmed its reliability. Two digital imaging biomarkers, Age Delta and Age Selta, were proposed and preliminarily validated in longitudinal cases as a proof-of-concept demonstration. This study primarily demonstrates the feasibility and potential clinical value of data-driven lumbar aging biomarkers.

Abstract Cardiac hypertrophy and fibrosis are common adaptive responses to injury and stress, eventually leading to heart failure. Hypoxia signaling is important to the (patho)physiological process of cardiac remodeling. However, the role of endothelial Prolyl-4 hydroxylase 2 (PHD2)/hypoxia inducible factors (HIFs) signaling in the pathogenesis of heart failure remains elusive. We observed a marked decrease of PHD2 expression in heart tissues and cardiovascular endothelial cells from patients with cardiomyopathy. Mice with Tie2-Cre-mediated deletion of Egln1 (encoding PHD2) or tamoxifen-induced endothelial Egln1 deletion exhibited left ventricular hypertrophy and cardiac fibrosis. Genetic ablation and pharmacological inhibition of Hif2a but not Hif1a in endothelial Egln1 deficient mice normalized cardiac size and function. The present studies define for the first time an unexpected role of endothelial PHD2 deficiency in inducing cardiac hypertrophy and fibrosis in a HIF-2α dependent manner. Targeting PHD2/HIF-2α signaling may represent a novel therapeutic approach for the treatment of pathological cardiac hypertrophy and failure. Brief Summary Endothelial PHD2 deficiency induces cardiac hypertrophy and fibrosis in a HIF-2α dependent manner. Targeting PHD2/HIF-2α signaling represents a novel therapeutic approach for the treatment of pathological cardiac hypertrophy and failure. Competing Interest Statement The authors have declared no competing interest.