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Biomedicines, Volume 14, Issue 6 (June 2026) – 5 articles

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34 pages, 3994 KB

Open AccessReview

Immunotherapy Landscape of Advanced Clear Cell Renal Cell Carcinoma: Targeting the Cancer-Immunity Cycle and Future Perspectives

by Xuanyu Jin, Junkai Yang, Daojia Miao, Wei Xiong and Zhiyong Xiong

Biomedicines 2026, 14(6), 1181; https://doi.org/10.3390/biomedicines14061181 (registering DOI) - 22 May 2026

Abstract

Renal cell carcinoma (RCC) is a predominant malignancy of the urinary system, with clear cell renal cell carcinoma (ccRCC) representing 75–85% of clinical cases. Since the early stages are often asymptomatic, nearly 30% of patients present with metastases at diagnosis, which significantly complicates the prognosis. The diverse mechanisms and clinical indications of current strategies, despite recent breakthroughs in immunotherapy, pose a major challenge for systematic application. This review employs the cancer-immunity cycle as a framework to evaluate four critical steps: antigen presentation, T-cell activation, reversal of exhaustion, and immune evasion in the tumor microenvironment. We introduce the major immunotherapy strategies in RCC in this cycle and summarize their clinical position. Combining immune checkpoint inhibitors (ICIs) with tyrosine kinase inhibitors (TKI) has redefined the first-line standard for advanced RCC by addressing both T-cell infiltration barriers and functional suppression. Standalone approaches such as tumor vaccines and cytokines in contrast have shown limited efficacy in advanced settings. In this context, we further propose emerging research directions, such as individualized immunotherapy and multi-target blockade, and point out the relevant biomarkers, offering an integrated perspective of the RCC immune landscape and providing insights for both clinical practice and future research. Full article

(This article belongs to the Special Issue Urological Oncology: Advances in Precision Diagnosis and Targeted Therapies)

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17 pages, 10323 KB

Open AccessArticle

Myeloid-Specific Deletion of Lnx2 Attenuates Estrogen-Deficiency-Induced Bone Loss by Inhibiting Osteoclastogenesis via the NUMB/NOTCH2 Axis

by Wei Wang, Jinhui Zhao, Ang Li, Chen Chen, Weitao Jia and Xiaolin Li

Biomedicines 2026, 14(6), 1180; https://doi.org/10.3390/biomedicines14061180 - 22 May 2026

Abstract

Background: We previously reported that knocking down the ubiquitin E3 ligase LNX2 in bone marrow monocytes by shRNAs attenuated osteoclastogenesis in vitro. However, the role of LNX2 in the regulation of osteoclasts and bone homeostasis in vivo remains unknown. Methods: In this study, we generated myeloid Lnx2 conditional knockout mice by crossing Lnx2-flox mice with LysM-Cre mice. The role of LNX2 was verified through in vitro osteoclast induction experiments using mononuclear macrophages and experiments on estrogen-deficient osteoporosis models. Results: Micro-CT and histological analysis unveiled that loss of Lnx2 in osteoclast precursor cells decreased osteoclast numbers and increased trabecular bone mass in mice. Moreover, Lnx2 deficiency prevented bone loss in an ovariectomized mouse model of postmenopausal osteoporosis. In vitro mechanistic studies identified that the loss of Lnx2 had little effect on cell proliferation but significantly inhibited the formation of osteoclasts and bone resorption. Furthermore, the deletion of Lnx2 decreased the expression of NOTCH2 and its downstream HES1 via enhancing the level of the NOTCH2 inhibitor, NUMB. Conclusions: Our findings elucidate an important role of Lnx2 in the regulation of osteoclasts and bone metabolism and indicate that Lnx2 is a potential therapeutic target for the treatment of osteoporosis. Full article

(This article belongs to the Topic Bone-Related Diseases: From Molecular Mechanisms to Therapy Development—2nd Edition)

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27 pages, 5927 KB

Open AccessArticle

Uncovering Novel Atrial Fibrillation Genetics Through Pleiotropic Overlap with Life’s Essential 8

by Jingxian Wu, Xueying Qin, Shuting Xie, Liuyan Zheng, Huan Yu, Huairong Wang, Yalin Chen, Teng Li, Tao Wu, Dafang Chen, Yonghua Hu and Yiqun Wu

Biomedicines 2026, 14(6), 1179; https://doi.org/10.3390/biomedicines14061179 - 22 May 2026

Abstract

Background/Objectives: Atrial fibrillation (AF) is a complex polygenic disorder; its genetic architecture remains challenging to fully elucidate. Methods: In this study, we leveraged the extensive genetic overlap between AF and a spectrum of cardiometabolic and behavioral factors—collectively defined by Life’s Essential 8 (LE8)—to advance our understanding of its etiology. Results: We first estimated significant genetic correlations between AF and all LE8 components (r_g: −0.11 to 0.19) using LD score regression. We then applied conditional false discovery rate analysis and detected 970 pleiotropic loci associated with AF and at least one LE8 trait. Subsequent colocalization analysis identified 179 loci harboring shared causal variants between AF and one or more LE8 components, which were further refined into 137 distinct colocalized regions. Through region-based annotation and functional predictors, we finally prioritized 164 candidate genes from these colocalized loci, including 40 novel genes. These candidate genes were enriched in pathways related to heart development and regulation of cardiac contraction, and were also enriched among molecular targets of otological agents. Among all LE8 components, blood pressure demonstrated the most extensive shared genetic architecture with AF, supported by the strongest genetic correlation, highest pleiotropic enrichment, and the greatest number of colocalized loci with AF. Polygenic risk scores constructed from these colocalized loci demonstrated significant associations not only for AF but also for arrhythmia and heart failure. Conclusions: Our findings establish a genetic pleiotropy-informed framework that enhances the discovery of novel risk loci of AF and advances our understanding of the shared genetic architecture and potential biological mechanisms between AF and LE8 components. Full article

(This article belongs to the Section Gene and Cell Therapy)

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13 pages, 1031 KB

Open AccessArticle

Insulin Resistance-Related Traits and Diabetic Maculopathy: Causal Insights from Mendelian Randomization

by Young Lee, Je Hyun Seo and Sung Pyo Park

Biomedicines 2026, 14(6), 1178; https://doi.org/10.3390/biomedicines14061178 - 22 May 2026

Abstract

Background/Objectives: To investigate the causal relationships linking body mass index (BMI) and circulating insulin-like growth factor 1 (IGF-1) levels with diabetic maculopathy risk using two-sample Mendelian randomization (MR). Methods: A two-sample MR framework was applied, utilizing genetic instruments for BMI and IGF-1 derived from the UK Biobank. Summary-level diabetic maculopathy data were obtained from the FinnGen consortium. Genome-wide significant single-nucleotide polymorphisms (SNPs, p < 5.0 × 10⁻⁸) independently associated with each exposure were employed as instrumental variables. Primary causal estimates were obtained using the inverse-variance weighted (IVW) method. Sensitivity analyses, including MR-Egger regression, weighted median methods, and the MR-Pleiotropy RESidual Sum and Outlier (MR-PRESSO), were conducted to evaluate robustness and potential pleiotropy. Results: Genetically predicted BMI was positively associated with diabetic maculopathy risk in both the IVW analysis (odds ratio [OR] = 1.16 (95% confidence interval [CI]: 1.04–1.30), p = 0.008) and MR-PRESSO (OR = 1.16 (95% CI: 1.04–1.28), p = 0.006). MR-PRESSO exhibited a significant relationship between higher IGF-1 levels and increased diabetic maculopathy risk (OR = 1.09 (95% CI: 1.01–1.18), p = 0.025), whereas the IVW method indicated only a suggestive association (OR = 1.08 (95% CI: 0.99–1.18), p = 0.087). Conclusions: The genetic evidence supports a causal role of insulin resistance-related traits in diabetic maculopathy development, with higher BMI and IGF-1 levels increasing diabetic maculopathy risk. These results underscore the potential contributory role of IGF-1 in disease pathogenesis and suggest that insulin resistance-related traits may represent preventive therapeutic targets. Full article

(This article belongs to the Special Issue Molecular Research on Diabetic Retinopathy (DR))

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11 pages, 557 KB

Open AccessArticle

Non-Criteria Antiphospholipid Antibodies in Women with Recurrent Pregnancy Loss

by Madina Khalmirzaeva, Gulfiruz Urazbayeva, Almagul Kurmanova, Nagima Mamedalieva, Gaukhar Kurmanova, Damilya Salimbayeva, Ainur Veliyeva, Gaini Anartayeva, Zhanar Kypshakbayeva, Shugyla Amirtayeva and Altynay Nurmakova

Biomedicines 2026, 14(6), 1177; https://doi.org/10.3390/biomedicines14061177 - 22 May 2026

Abstract

Background: Recurrent pregnancy loss (RPL) remains etiologically unexplained in 40–50% of cases following standard diagnostic workup. Non-criteria antiphospholipid antibodies (non-criteria aPL) are increasingly considered potential markers of seronegative obstetric antiphospholipid syndrome (APS); however, their diagnostic value in this clinical setting requires further investigation. Objective: To assess the diagnostic value of non-criteria aPL in women with RPL and to construct an exploratory immunological scoring model for diagnostic stratification. Methods: Antiphospholipid antibody detection was performed using a single-measurement semi-quantitative line immunoblot assay (Anti-Phospholipid 10 Dot, Generic Assays, Germany). Statistical analysis included χ², Fisher’s exact test, Mann–Whitney U test, binary logistic regression, and ROC analysis. Results: Statistically significant associations with RPL were observed for anti-prothrombin antibodies (OR = 11.1; 95% CI 1.8–68.0; p = 0.022 [Haldane–Anscombe correction]), anti-annexin V (OR = 4.28; 95% CI 1.18–15.6; p = 0.023), and anti-β₂GP I (OR = 3.31; 95% CI 1.18–9.28; p = 0.019). The exploratory composite immunological score demonstrated moderate discriminatory performance (AUC = 0.701; 95% CI 0.588–0.814; p = 0.005). The overall logistic regression model was statistically significant (χ² = 8.564; p = 0.036), although none of the individual predictors retained independent significance, indicating a contribution of cumulative immunological burden rather than any single marker. Conclusions: In this single-center cross-sectional study, non-criteria aPL were frequently detected in women with RPL and were statistically associated with the condition. The findings should be interpreted as hypothesis-generating only, given the cross-sectional design, single-measurement immunoblot, small control group, and absence of external validation. Confirmation in larger prospective multicenter cohorts using ELISA-based assays with the internationally recommended 12-week repeat measurement is required before any clinical implementation. Full article

(This article belongs to the Special Issue Immunology in Recurrent Pregnancy Loss, Preeclampsia and Infertility)

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