Following the publication of the above paper, it was drawn to the Editor's attention by an interested reader that an unsuitable antibody may have been used as a part of the western blot analysis shown in Fig. 3A on p. 720. The anti‑β‑galactosidase antibody (cat. no. ab9361; Abcam) that was employed, which is specific for the E. coli β‑galactosidase encoded by the LacZ gene; is only distantly related to the human protein, and would not necessarily be expected to bind to it. The authors have been contacted by the Editorial Office to offer an explanation for the selection of this apparently unsuitable antibody for the western blot analysis, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of a potential problem surrounding the design of this experiment in this study, we are issuing an Expression of Concern to notify readers of this issue while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 43: 717‑726, 2019; DOI: 10.3892/ijmm.2018.4005].

Immune checkpoint inhibitors have changed cancer treatment, although durable benefit remains limited because malignant, immune and stromal cells sustain suppression within the tumor immune microenvironment. Extracellular vesicles (EVs), including small EVs, can transfer circular RNAs (circRNAs) between defined donor and recipient cells. The relevant steps extend from circRNA biogenesis and entry into EV populations to delivery, intracellular activity, immune phenotype and clinical use. Incomplete transfer experiments, tumor‑intrinsic circRNA activity and engineered RNA platforms differ from direct EV‑mediated transfer. Direct transfer has been linked to tumor‑associated macrophages, myeloid‑derived suppressor cells, natural killer cells, CD8+ T cells and regulatory T cells. Within recipient cells, circRNAs can regulate microRNA availability, assemble RNA‑binding protein complexes, alter protein or RNA stability and produce functional peptides. Donor state, recipient identity, tissue site, EV subpopulation and delivered dose can change the resulting phenotype. Cancer‑associated fibroblasts further connect EV‑associated circRNAs with matrix remodeling, immune‑cell access and treatment tolerance. Biological support is classified from E0 to E3, while EV methods are considered separately through source definition, separation, characterization, RNA protection, uptake controls and quantitative dose. Translation will require full‑length circRNA identification, absolute measurement in EVs and recipient cells, spatial localization, prospective treatment cohorts and repeated‑dose safety testing. These requirements distinguish circulating associations from transferred molecules and identify the experiments needed for biomarker or therapeutic development.

In recent years, with the deepening understanding of the significant role of small non‑coding RNAs in human health and diseases, transfer RNA‑derived RNAs (tsRNAs) have gradually become a research focus. Existing evidence shows that tsRNAs not only participate in the regulation of liver gene expression, translation and stress response, but may also act as signaling molecules to mediate inter‑organ communication. However, the specific pathological mechanism and clinical value in the occurrence and development of liver diseases remain unclear. Although tsRNAs show promising prospects as non‑invasive biomarkers and are expected to be used in the diagnosis of liver diseases, screening of therapeutic targets, drug delivery and regulation of enzyme activity, the methodological limitations at present and the differences in performance among different disease types and populations have significantly restricted their clinical translation. The present article systematically reviews the pathological roles of tsRNAs in various liver diseases, with a focus on elaborating their roles in tumor evolution, metabolic disorders and immune regulation. Their clinical application potential was also evaluated, methodological challenges were discussed, and future directions were proposed to advance tsRNA‑based clinical translation in hepatology.

Following the publication of the above article, an interested reader raised several comments on the study that required clarification on the part of the authors in order to confirm the reporting of certain of the results, and to make the paper fully comprehensible. First, in the Materials and methods section, the single‑cell RNA sequencing (RNA‑seq) source did not appear to match the presented groups for the scRNA‑seq data that were obtained from the GSE116222 dataset, specifically using 'three human UC samples', where three distinct groups, namely the 'Normal', 'Non‑inflamed' and 'Inflamed' groups, were shown in various of the figures (for example, Fig. 1D and Fig. 6K). Secondly, the description of the Weighted Gene Co‑expression Network Analysis (WGCNA) in the Materials and methods section did not tally with the findings reported in the Results section. It was stated in the 'Construction of co‑expression network' subsection of the Methods that WGCNA was performed 'based on the GSE116222 dataset, specifically exploring the association between FXR and CD133 in intestinal cells'; however, all the WGCNA results shown (in Figs. 4D and 5A) were based on the bulk transcriptome dataset GSE87466, not on single‑cell data; no WGCNA output from GSE116222 was presented in the paper. Thirdly, some confusion between human and mouse data appeared in the reporting of the experiments in Fig. 1E. The figure part showed macroscopic photographs of whole large intestines and spleens labeled 'Control' and 'UC groups', and these images must have been derived from the DSS‑treated mouse model. The figure legend did not specify that these are mouse data, and the labeling of the 'UC group' was misleading. Finally, a typographical error in the reporting of the human control group sex distribution was contained in the 'Human sample collection and processing' subsection: 'the control group consisted of 8 men and 2 men' was presumably intended to have read as '8 men and 2 women'. The authors have considered these points, and acknowledge that clarifications of all of them are necessary in the published paper; therefore, the following changes and edits to the text are required (all highlighted in bold). First, in the 'Materials and methods' section, in the 'Single‑cell RNA sequencing (scRNA‑seq)' subsection, the text which read as 'scRNA‑seq data from three human UC samples were downloaded from the Gene Expression Omnibus (GEO) database...' has now been changed to 'scRNA‑seq data from 9 samples (3 healthy, 3 non‑inflamed, and 3 UC) were downloaded from the Gene Expression Omnibus (GEO) database...' In response to the second of the reader's queries, in the 'Construction of co‑expression network' subsection of the Methods, the text which read: 'In the present study, the 'WGCNA' package in R was employed to construct a co‑expression network based on the GSE116222 dataset, specifically exploring the association between FXR and CD133 in intestinal cells.', should be changed to: 'In the present study, the 'WGCNA' package in R was employed to construct a co‑expression network based on the GSE87466 dataset to identify key gene modules associated with UC.' In response to the third query, and to properly clarify the descriptions of the experiments in the figure legend for Fig. 1, the text for Fig. 1E should be changed from what was written to the following: '(E) Representative macroscopic images of the large intestines and spleens from the Control and DSS groups.' (i.e., 'UC groups' has been corrected to 'DSS groups'). Finally, the authors acknowledged that a typographical error was present in the reporting of the human control group sex distribution in the 'Human sample collection and processing' subsection, and the text here should have read as 'the control group consisted of 8 men and 2 women (mean age, 46.2±7.5 years).' The authors thank the reader for drawing these matters to their attention. They are grateful to the Editor of International Journal of Molecular Medicine for granting them the opportunity to publish this corrigendum. Note that the proposed changes to the text only correct errors in what was written, or clarify the meaning of the text; the results and conclusions of the paper are not affected by these changes. Finally, the authors apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 58: 200, 2026; DOI: 10.3892/ijmm.2026.5871].

Glaucoma consists of a group of neurodegenerative diseases characterized by retinal ganglion cell degeneration, in which Müller cells are increasingly recognised as drivers of neuroinflammation. A ketogenic diet (KD) elevates circulating β‑hydroxybutyrate (BHB) and exhibits benefits in other neurodegenerative disorders; however, its role in glaucoma remains poorly understood. In the present study, an experimental autoimmune glaucoma (EAG) mouse model was established and primary Müller cells were cultured. Using spectrophotometry, optical coherence tomography and immunofluorescence, serum ketone body levels were found to be significantly lower in both patients with primary open‑angle glaucoma and EAG mice, independent of intraocular pressure. In vitro and in vivo experiments showed that KD increased BHB levels and ketone body metabolism, suppressed Müller cell activation and reduced retinal neuroinflammation. In addition, 4D data‑independent acquisition proteomic analysis and subsequent validation revealed that FOXO3A acetylation and FOXO3A and metallothionein 2A upregulation were regulated in the retina and Müller cells. These findings suggest that impaired ketone body metabolism occurs in glaucoma and that KD‑mediated neuroprotection is associated with altered FOXO3A acetylation. The present study highlighted an association between ketone metabolism and immune regulation in glaucoma, providing evidence for Müller cell phenotypic modulation and supported further investigation of KD as a potential neuroprotective adjunct therapy for glaucoma.

Osteoarthritis (OA) is a progressive degenerative joint disease and a leading cause of pain, disability and loss of joint function in older adults worldwide. Small extracellular vesicles (sEVs) are small vesicles secreted by cells and found in various body fluids. They carry a range of bioactive molecules, including nucleic acids, proteins and lipids, and participate in numerous cellular physiological activities, such as cell death, inflammation, immunity, proliferation, migration and differentiation. Depending on their cellular origin, sEVs can exert opposing effects on OA: They may either aggravate inflammation and cartilage damage or suppress inflammation and promote cartilage repair. Therefore, this review focuses on the preclinical research evidence regarding the dual mechanism of 'promoting or treating' by sEVs in the disease of OA, aiming to construct a theoretical framework to provide a theoretical basis for the development and translational application of OA treatment strategies based on sEVs.

Pneumonia remains one of the most prevalent and deadly respiratory diseases worldwide, imposing substantial clinical and socioeconomic burdens. Monocytes (Mos) and their progeny are key components of the innate immune system and perform highly context‑dependent roles. The present review summarizes recent advances in understanding Mo biology in pneumonia and discusses current concepts of their functional plasticity. The review first summarizes the developmental origins, phenotypic heterogeneity and functions of circulating Mo subsets, followed by an overview of their recruitment, activation and differentiation in the steady‑state and infected lung. Next, the dual, and at times opposing, roles of Mos and their progeny in pneumonia are examined, including contributions to pathogen clearance and microbial immune evasion, the initiation and resolution of inflammation, and tissue repair vs. fibrotic remodeling. Finally, the review highlights emerging evidence showing that pneumonia can induce durable innate immune memory in Mos, their progenitors and the alveolar macrophage compartment. This reprogramming may reshape subsequent pulmonary and systemic immune responses, with important implications for susceptibility to reinfection, chronic lung dysfunction and host resilience. A deeper understanding of Mo plasticity and innate memory may open new avenues for biomarker discovery and host‑directed therapeutic strategies for pneumonia.

Type 3 innate lymphoid cells (ILC3s) constitute key components of mucosal innate immunity and serve key roles in maintaining mucosal barrier homeostasis and regulating inflammatory responses. The present review summarizes the biological characteristics and regulatory mechanisms of ILC3s, while discussing their interactions with the gut microbiota and pathological functions in mucosa‑associated disorders. Derived from bone marrow‑resident common lymphoid progenitors, ILC3s differentiate under the transcriptional control of retinoid‑related orphan receptor γ‑t into distinct functional subsets, including natural cytotoxicity receptor (NCR)+ ILC3s, NCR‑ ILC3s and lymphoid tissue inducer cells. ILC3s maintain epithelial barrier integrity, enhance antimicrobial defense and support lymphoid tissue development through the production of effector molecules such as IL‑22, IL‑17 and granulocyte‑macrophage colony‑stimulating factor. These subsets can undergo phenotypic conversion in response to microenvironmental signals. ILC3 activity is tightly regulated by transcription factors, metabolic pathways, neuroimmune interactions and the circadian clock system. In addition, ILC3s establish bidirectional interactions with the gut microbiota: Microbial metabolites regulate ILC3 activity, whereas ILC3s influence microbial composition through IL‑22‑dependent antimicrobial peptide production and IgA responses. Depending on subset composition, local cytokine networks and tissue microenvironment, ILC3s may exert either pathogenic or protective effects in a number of diseases. Future investigations should aim to further elucidate the molecular mechanisms underlying ILC3 subset plasticity, tissue‑specific interaction networks and clinically translatable strategies for targeted intervention. Building upon these findings, the present review proposes a spatiotemporal‑quantitative framework and three regulatory axes that may account for disease‑specific variations in ILC3 responses, providing a basis for understanding distinct ILC3 functions and developing targeted therapeutic strategies. Systematic investigation of the regulatory principles governing ILC3 biology will not only deepen the understanding of innate immune homeostasis but also provide potential targets and strategies for precision immunotherapy in diseases such as inflammatory bowel disease and colorectal cancer.

Following the publication of the above paper, a concerned reader drew the Editor's attention to the fact that a number of data panels shown for the cell migration assay data in Fig. 1C on p. 1238 and Fig. 3A on p. 1240 appeared to contain overlapping sections, such that data which were intended to show the results of differently performed experiments were apparently derived from a much smaller number of original sources. The authors were contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, and they have replied to confirm that Figs. 1 and 3 were assembled incorrectly; moreover, although the overlapping images appeared to represent different fields of view, the authors suspected that the errors may have occurred when misfiled images were inserted from the wrong folder during figure preparation. In addition to the issues with Figs. 1 and 3, and even though there were no obvious issues of data mishandling present, the authors also declared that they were unable to retrieve the original experimental data relating to the cell migration assay experiments shown in Fig. 4. The authors requested that the cell migration experiments pertaining to Figs. 1, 3 and 4 be repeated, and the Editor agreed to the authors' request. The revised versions of Figs. 1, 3 and 4, now showing new data for Figs. 1C, 3A and 4B, together with new histograms that have been prepared for the re‑quantification of the new data, are shown on the next two pages. Note that the results obtained from the newly performed experiments were broadly similar to the originally published results, and therefore the revisions made to these three figures have not grossly affected either the results or the conclusions reported in this study. All the authors agree with the publication of this Corrigendum, and they are grateful to the Editor of International Journal of Molecular Medicine for granting them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 33: 1236‑1242, 2014; DOI: 10.3892/ijmm.2014.1661].

The fate of CD8[+] T cells is dictated by epigenetic remodeling, metabolic rewiring and most critically, the transcriptional reprogramming that integrates diverse extracellular signaling pathways. Transcription factors (TFs) predetermine cell differentiation state and lineage‑specifying hub TFs are decisive for CD8[+] T cell functional maturation. The present study aimed to summarize the indispensable roles of interferon regulatory factors (IRFs) in CD8[+] T cell biology from early thymic development to the acquisition of distinct functional states. Alone or together with other TFs, IRFs are involved in the regulation of CD8[+] T cell commitment, effector differentiation, memory maintenance and terminal exhaustion. In clinical practice, IRF family members hold potential as prognostic biomarkers and valuable therapeutic targets in CD8[+] T cell‑associated immune disorders, such as tumors, transplant rejection, infection and autoinflammatory diseases.

Heatstroke is a life‑threatening condition characterized by hyperthermia and systemic inflammatory response, often leading to multi‑organ dysfunction and high mortality. Despite advances in understanding its pathophysiology, effective targeted therapies remain limited. Recent studies have highlighted ferroptosis, an iron‑dependent, lipid peroxidation‑driven form of regulated cell death, as a critical mechanism in heatstroke‑induced organ injury. This review synthesizes current evidence on the role of ferroptosis in heatstroke, including key signaling pathways such as Hippo‑Yes‑associated protein‑acyl‑CoA synthetase long‑chain family member 4, dysregulated heat shock response, and antioxidant defense failure. The present study also explored potential ferroptosis‑related biomarkers and therapeutic strategies targeting this cell death pathway. Understanding ferroptosis in heatstroke not only unveils novel pathophysiological insights but also opens avenues for early diagnosis and targeted intervention.

Following the publication of the above paper, it was drawn to the Editor's attention by an interested reader that a pair of unsuitable antibodies may have been used as a part of the western blot analysis shown in Fig. 1E on p. 1314. First, the antibody with the catalogue number ab51243 (purchased from Abcam), is not specific for p16‑INK4a (the senescence‑associated protein studied in this paper), but a totally different protein with a similar name, p16‑ARC. A concern was also raised regarding the anti‑β‑galactosidase antibody (cat. no. ab9361; Abcam) that was employed, which is specific for the bacterial protein and is only distantly related to human β‑galactosidase according to its sequence (neither is this antibody the closest homologue to bacterial β‑galactosidase in the human proteome). The authors have been contacted by the Editorial Office to offer an explanation for the selection of these apparently unsuitable antibodies for the western blot analysis, and we are awaiting their response. Owing to the fact that the Editorial Office has been made aware of a potential problem surrounding the design of these experiments in this study, we are issuing an Expression of Concern to notify readers of this issue while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 43: 1311‑1320, 2019; DOI: 10.3892/ijmm.2019.4074].

Knee osteoarthritis (KOA) is a chronic, disabling disease with multiple etiologies and a complex pathophysiology. Conservative treatment is the cornerstone of KOA management, and when it proves insufficient, extracorporeal shock wave therapy (ESWT) has emerged as a practical non‑invasive alternative. The present narrative review systematically summarizes current preclinical and clinical evidence on ESWT for KOA through a structured literature search, aiming to integrate its therapeutic effects and identify knowledge gaps. Accumulating evidence indicates that ESWT can slow KOA progression through multiple biological pathways, encompassing anti‑inflammatory, anti‑apoptotic, pro‑proliferative and cartilage‑protective effects, while also relieving pain and improving function clinically. Summarizing the available data, this review finds that ESWT exhibits a favorable safety profile for articular tissues and disease‑modifying potential in preclinical models, although treatment outcomes depend critically on energy flux density and protocol selection. In human studies, the current evidence primarily supports symptomatic relief, including pain reduction and functional improvement; high‑quality trials with structural endpoints to verify cartilage regeneration or joint space preservation remain scarce. Given its non‑invasive nature, safety and growing clinical support, ESWT merits consideration as an adjunctive therapy. However, heterogeneity in treatment parameters and limited long‑term data preclude standardized guidelines. Despite these limitations, ESWT remains a promising adjunctive therapy for patients who are unresponsive to conventional conservative treatments. Future research should prioritize parameter optimization, extended follow‑up and translational studies to bridge the gap between preclinical structural findings and clinical application. Addressing these gaps will strengthen the therapeutic role and scientific foundation of ESWT.

Following the publication of the above article, a concerned reader drew the Editor's attention to the fact that, regarding the EdU assay experiments shown in Fig. 6 on p. 657, discrete areas of the cells appeared to overlap in different data panels, which were intended to show differently performed experiments in two distinct cell lines (the SW1990 and Panc‑1 cell lines), albeit the areas were inverted in the case of the 'LV‑RNAi' data panels. Moreover, within these areas of overlapping cells, certain of the cells were uniquely found to be coloured differently in the associated data panels. In addition, in Fig. 9 on p. 658, the bands shown for the caspase‑3 and caspase‑3 experiments with the SW1990 cell line looked remarkably similar, suggesting that the data in this figure may also have been assembled incorrectly. After having conducted an internal investigation of the data in this paper, the Editor of International Journal of Molecular Medicine has decided that this article should be retracted from the publication on the grounds of an overall lack of confidence in the presented data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 32: 653‑660, 2013; DOI: 10.3892/ijmm.2013.1437].

Salvianolic acids (SAs), a water‑soluble active component extracted from the traditional Chinese herb Salvia miltiorrhiza, have attracted considerable attention as an anti‑tumor agent. Accumulating evidence demonstrates that SAs potently inhibit tumor‑cell migration, invasion and metastasis through multiple signaling pathways and molecular targets. First, SAs remodel the extracellular matrix and suppress matrix metalloproteinase activities, thereby attenuating the epithelial‑mesenchymal transition and the associated stem‑like properties of cancer cells. Second, SAs block tumor angiogenesis, depriving tumors of essential nutrients and routes for metastasis. Third, SAs reprogram the tumor microenvironment by modulating immune cells, enhancing immune cell infiltration and relieving immunosuppression, ultimately curbing tumor progression. Fourth, SAs target metastatic cellular plasticity and therapy resistance by disrupting cytoskeletal reorganization, impairing cell motility and reversing drug‑resistant phenotypes, thereby enhancing cancer treatment efficacy with reduced toxicity. At the molecular level, SAs suppress the PI3K/AKT, MAPK and TGF‑β1/Smad signaling cascades, thereby diminishing the invasive and migratory capacity of tumor cells. In this review, recent advances in understanding the anti‑metastatic effects and underlying mechanisms of SAs were systematically summarized, the challenges hindering their clinical translation were discussed and future directions that may facilitate their development as a promising anti‑metastatic therapeutic agent were outlined.