<p>Following the publication of the above article and an expression of concern statement (doi: 10.3892/ijmm.2025.5680) after it had been drawn to the Editor's attention by an interested reader that, regarding the western blot data shown in Fig. 5 on p. 507, the first set of GAPDH bands for the GH3 cell line were strikingly similar to the EGFR protein bands shown for the GT1‑1 cell line in the adjacent set of gels, the authors have now replied to the Editorial Office to explain the apparently anomalous appearance of this figure. After having examined their original data, the authors have realized that this figure was assembled incorrectly; essentially, the wrong data were included in this figure to portray the GAPDH bands for the GH3 cell line. The revised version of Fig. 5, now showing the correct GAPDH data for the GH3 cell line, is featured on the next page. The authors can confirm that the error made during the assembly of Fig. 5 did not have a significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of International Journal of Molecular Medicine for allowing 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 47: 500‑510, 2021; DOI: 10.3892/ijmm.2020.4807]</p>.

<p>Hepatic stellate cells (HSCs), specialized liver‑resident pericytes, play pivotal roles in both liver fibrogenesis and regeneration. Following hepatic injury, quiescent HSCs undergo activation and transdifferentiation into myofibroblasts, which drive tissue remodeling and scar formation. Recent advances have uncovered notable phenotypic and functional heterogeneity within HSC populations, with distinct subsets displaying context‑dependent activation states and specialized functions across diverse liver pathologies. The present review synthesizes current insights into the dynamic spectrum of HSC phenotypes and the molecular mechanisms governing their plasticity, emphasizing the mechanisms through which niche‑specific signaling, epigenetic regulation and metabolic reprogramming coordinate their functional diversity. The present review further discuss emerging therapeutic strategies that leverage this heterogeneity to selectively target pathogenic HSC subsets, while preserving their homeostatic roles, thereby opening new avenues for precision anti‑fibrotic therapies and liver regeneration.</p>.

<p>Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by marked genetic heterogeneity and diverse environmental influences. Current treatment approaches focus on symptom management, with only a limited number of effective interventions targeting the underlying causes. Recently, mesenchymal stem cells (MSCs) and their derived exosomes (MSC‑Exos) have emerged as promising candidates for ASD therapy owing to their potent immunomodulatory, neuroprotective and targeted delivery properties. The present review discusses the functions of MSC‑Exos and their potential use in ASD. MSC‑Exos improve neuroinflammation, enhance synaptic plasticity and restore neural network function by delivering bioactive molecules. Moreover, MSC‑Exos exhibit a low immunogenicity, a favorable safety profile and scalability for clinical production. Despite promising results however, clinical trials continue to face challenges, particularly in standardizing the isolation, characterization, dosing and administration routes of exosomes. In addition, significant challenges persist in production processes, quality control and the elucidation of the mechanisms of action. In conclusion, MSC‑Exos represent a groundbreaking, cell‑free therapeutic strategy with substantial potential to target the core pathophysiology of ASD. In the future, multicenter randomized controlled trials and interdisciplinary collaborations will be crucial for translating preclinical findings into the development of effective and transformative therapies for ASD.</p>.

<p>Following the publication of this article, a concerned reader drew to the Editor's attention that the image showing silica nanoparticles in Fig. 1 on p. 906 had also been used to show the same data in another paper published by the same research group in International Journal of Molecular Medicine. Upon performing a separate investigation of the data in this paper in the Editorial Office, it also came to light that flow cytometric plots featured in Fig. 3 on p. 908 had originally been included in a paper featuring some of the same authors that had already been published in International Journal of Nanomedicine, and western blot data featured in Fig. 7 on p. 910 were originally included in another paper featuring some of the same authors in the journal Stem Cell Research & Therapy. Given the apparent re‑use of the abovementioned data in this article from previously published papers, the Editor of International Journal of Molecular Medicine has decided that this article should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 44: 903‑912, 2019; DOI: 10.3892/ijmm.2019.4265]</p>.

Zymogen granule protein 16B (ZG16B), also known as pancreatic adenocarcinoma upregulated factor, is a secretory lectin-like glycoprotein that serves a crucial role in tumorigenesis and immune regulation. The present review summarizes the latest research progress on the molecular characteristics, biological functions, signaling pathway regulation and clinical importance of ZG16B. Structurally, ZG16B contains an N-terminal hydrophobic signal peptide, a jacalin-related lectin domain and a C-terminal extension. Functionally, ZG16B promotes tumor cell proliferation, migration, invasion and angiogenesis, and increases vascular permeability by activating the Toll-like receptor, C-X-C chemokine receptor type 4, β-catenin and focal adhesion kinase signaling pathways. In the tumor microenvironment, ZG16B can modulate immune responses, enhance the immunosuppressive functions of myeloid-derived suppressor cells and M2 macrophages, and also promote the maturation of dendritic cells. Clinically, ZG16B expression is upregulated in pancreatic cancer, ovarian cancer, colorectal cancer, gastric cancer and oral cancer, and its upregulation is associated with a worse prognosis in these malignancies. Several ZG16B-specific therapeutic strategies, including monoclonal antibodies, RNA aptamers and trans-splicing ribozymes, have shown preclinical efficacy against malignant tumors. Furthermore, a clinical trial is currently testing the efficacy and safety of PBP1510, a humanized ZG16B antibody, for the treatment of advanced pancreatic cancer. In conclusion, ZG16B may be considered a novel target for cancer diagnosis, prognosis and therapy.

Following the publication of this article, a concerned reader drew to the Editor's attention that the image showing silica nanoparticles in Fig. 1 on p. 1232 had also been used to show the same data in another paper published by the same research group in International Journal of Molecular Medicine. Upon performing a separate investigation of the data in this paper in the Editorial Office, it also came to light that, concerning the immunohistochemical images shown in Fig. 8A on p. 1236, five pairs of data panels out of a total of 12 panels included in this figure contained overlapping sections of data, occasionally in different orientations with respect to other panels, such that data which were intended to show the results from differently performed experiments had apparently been derived from a smaller number of original sources. Given the large number of panels in this figure that were revealed to have overlapping sections, the Editor of International Journal of Molecular Medicine has decided that this article should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 43: 1229‑1240, 2019; DOI: 10.3892/ijmm.2018.4045].

During antiviral immunity, MHC‑I molecules display endogenous peptides to CD8+ T‑cell receptors, prompting cytotoxic elimination of infected cells. The present study focused on dominant epitopes derived from the nucleocapsid protein (NP) of Hantaan virus (HTNV) and revealed their high affinity for the HLA‑I and H‑2 superfamilies. Through immunogenicity and conservation analyses, four selective epitopes were precisely identified. Molecular docking validated the binding characteristics of selective epitopes with MHC‑I molecules. Bidirectional hierarchical clustering analysis uncovered complex interaction patterns between NP 9‑mer peptides and MHC‑I haplotypes. Moreover, in‑depth investigation of 11 HTNV variants revealed three amino acid substitutions (I241S, E242A and F384I) within the four selective epitopes; however, these substitutions did not significantly affect the pan‑HLA‑I immunoreactivity of these epitopes. Safety assessments highlighted the potential of four selective epitopes for practical applications. Utilizing ELISpot, ELISA and flow cytometry, the immunogenicity of these selective epitopes was comprehensively confirmed. In summary, the present study thoroughly evaluated the pan‑MHC‑I immunoreactivity of HTNV NP, providing a robust foundation for developing effective epitope vaccines for population immunity.

As a key component of the immune system, B cells primarily mediate humoral immunity via the synthesis and secretion of antibodies. In addition, B cells contribute to immune responses via antigen presentation and cytokine secretion. B cell‑targeted therapy has potential for the treatment of autoimmune diseases. However, current B cell‑targeted therapies have limited efficacy when used as monotherapies in clinical settings. In an aim to provide in‑depth understanding of this limitation, the present review discusses the developmental and differentiation pathways of B cells and the mechanisms by which various B cell subsets participate in immune responses, as well as randomized controlled trials on B cell‑targeted therapies conducted on lupus nephritis, an autoimmune disease with a notable inflammatory response. The clinical benefits of these therapies remain modest. This suggests that while B cells may serve a pathogenic role, existing therapies fail to address the fundamental mechanisms underlying disease progression. Targeting the interactions between B and T cells, particularly by inhibiting B cell‑mediated antigen presentation, may represent a promising novel direction for B cell‑targeted therapy.

Following the publication of this paper, it was drawn to the Editor's attention by an interested reader that, for the western blot experiments shown in Fig. 7A on p. 405, the Bcl‑2 and PCNA blots for the SO‑Rb50 cell line appeared to be identical, albeit it with possibly slightly different exposure time of the gel and different vertical dimensions. Similarly, the BAX and PCNA blots for the Y79 cell line also appeared to be identical, although the blots were rotated by 180° relative to each other, again with possibly slightly different exposure time of the gel and different vertical dimensions. In addition, for the experiments showing transfection efficiency in Fig. 1 on p. 402, the 'SO‑Rb50/x100/PAX6‑RNAi GFP' and 'Y79/x200/Ctrl GFP' data panels contained overlapping data, and the 'SO‑Rb50/x200/PAX6‑RNAi GFP' and 'Y79/x100/Ctrl GFP' data panels similarly contained overlapping data, suggesting that these pairings of panels had been placed in this figure the wrong way around. Upon contacting the authors about these issues, they realized that Figs. 1 and 7 in this paper had inadvertently been assembled incorrectly. The revised versions of Fig. 1, now featuring the correct data for the PCNA blots for both the SO‑Rb50 and the Y79 cell lines, and Fig. 7, now showing the correctly positioned data panels for the 'SO‑Rb50/x100/PAX6‑RNAi GFP' and 'Y79/x200/Ctrl GFP' experiments, are presented on the next page. The authors wish to emphasize that the errors made in assembling the data in these Figures did not affect the overall conclusions reported in the paper. The authors are grateful to the Editor of International Journal of Molecular Medicine for granting them this opportunity to publish a Corrigendum, and apologize to both the Editor and the readership for any inconvenience caused. [International Journal of Molecular Medicine 34: 399‑408, 2014; DOI: 10.3892/ijmm.2014.1812].

Air pollution, an emerging global environmental issue, alongside extreme meteorological conditions exacerbated by climate change, threaten the sustainability of modern society and contribute to the onset and progression of various ear and nose diseases. Nonetheless, the impact of these environmental factors on ear and nose diseases and related dysfunctions remain inadequately explored. The present review involved a comprehensive search of PubMed, Web of Science, the Cochrane Library and Embase for relevant epidemiological and experimental data. How environmental factors contribute to olfactory and auditory system dysfunctions as well as the potential underlying mechanisms from the perspectives of immunity and inflammation were examined in the present review. It was found that air pollution and meteorological factors significantly influence the prevalence of major ear and nose diseases, including allergic rhinitis, otitis media and sudden sensorineural hearing loss. Of note, the present review also provides an examination of the interaction between severe acute respiratory syndrome coronavirus 2 and environmental factors in ear and nose diseases, highlighting how environmental stressors may worsen disease progression. In conclusion, the present review underscores the burden of multimorbidity caused by air pollution and extreme weather and emphasizes the need for more targeted prevention and management strategies for ear and nose diseases.