International journal of molecular medicine最新文献

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].

Following the publication of this paper, a concerned reader drew to the Editor's attention that, according to a study published by Kristin Entrop and colleagues in the journal Cell Death & Disease in 2024, an unspecific anti‑Bax antibody (sc‑7480) had been used in the above study, which was shown to bind to an unrelated protein at the correct molecular weight (20‑25 kDa). Furthermore, it also came to light that, for the cell migration and invasion assay data shown in Fig. 8B on p. 10, at least four pairs of data panels were shown to feature overlapping sections, such that data which were intended to show the results of differently performed experiments had apparently been derived from a smaller number of original sources. After having performed an independent review of the data in the Editorial Office, the Editor of International Journal of Molecular Medicine has decided that this paper should be retracted from the Journal on account of a 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 apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 47: 69, 2021; DOI: 10.3892/ijmm.2021.4902].

Atherosclerosis (AS), a chronic vascular pathology characterized by endothelial dysfunction, arises from the interplay of lipid dysregulation, oxidative stress, and inflammatory activation. Reactive oxygen species (ROS) overproduction triggers Nod‑like receptor protein 3 (NLRP3) inflammasome signaling, exacerbating inflammatory cascades that drive plaque progression. The nuclear factor erythroid 2‑related factor 2 (Nrf2)‑mediated antioxidant pathway serves as a critical counterbalance to ROS/NLRP3 axis dysregulation, positioning pharmacological Nrf2 activation as a promising therapeutic strategy. The present study investigated the anti‑atherosclerotic potential of ginkgolide C (GC), a terpene lactone from Ginkgo biloba with established anti‑inflammatory and anti‑ischemia/reperfusion injury properties, through coordinated modulation of redox‑inflammatory pathways. Complementary in vivo (high‑fat diet/vitamin D3‑treated ApoE-/- mice) and in vitro (oxidized‑low density lipoprotein‑stimulated aortic endothelial cells) models were established. Comprehensive analyses included histopathological characterization, lipid profiling, ultrastructural examination, redox‑inflammatory biomarker quantification, and molecular pathway validation. GC significantly attenuated hyperlipidemia and plaque progression while preserving vascular ultrastructure. Mechanistically, GC enhanced endothelial survival through dual pathway modulation: i) Nrf2 nuclear translocation upregulated antioxidant enzymes [heme oxygenase‑1/NAD(P)H quinone oxidoreductase 1/glutamate‑cysteine ligase modifier subunit], restoring redox homeostasis; ii) NLRP3 inflammasome inhibition via Caspase‑1 suppression mitigated inflammatory cytokine release. The present study demonstrated GC's dual‑target therapeutic efficacy against AS through Nrf2‑mediated oxidative stress resolution and NLRP3 inflammasome inactivation, offering new insights into phytochemical‑based cardiovascular interventions.

Cognitive impairment remains an important global health concern, with the molecular mechanisms regulating its progression being a primary research focus. Ferroptosis, a unique form of programmed cell death characterized by iron‑dependent lipid peroxidation, has been increasingly recognized for its essential role in the progression of various neurodegenerative diseases and diabetes‑associated cognitive impairment. The present review summarizes current evidence on how ferroptosis contributes to cognitive decline and outlines its regulation through lipid, iron and glutathione metabolism; it further discusses how diverse upstream pathologies converge on ferroptosis as a shared mechanism underlying cognitive dysfunction. In addition, recent advances in ferroptosis‑related biomarkers and therapeutic strategies are highlighted, with the aim of providing a clearer framework for understanding its pathogenic roles and guiding future clinical translation.

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.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that a pair of the data panels shown for the Masson staining experiments in Fig. 3A were overlapping, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. Upon performing an independent analysis of the data in this paper in the Editorial Office, it came to light that a pair of the panels in Fig. 4A also contained overlapping sections of data, and moreover, the data in Fig. 3A were strikingly similar to data which had appeared in a number of other articles that were written by different authors at different research institutes, several of which have been retracted, including one that had been published prior to the reciept of the above paper to International Journal of Molecular Medicine. Owing to the fact that the contentious data in the above article were found to be strikingly similar to data that had already been published elsewhere, the Editor of International Journal of Molecular Medicine has decided that this paper 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: 49‑760, 2019; DOI: 10.3892/ijmm.2018.4034].

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 paper, it was drawn to the Editor's attention by a concerned reader that the control GAPDH western blots featured in Fig. 5A and B on p. 2845 were apparently the same (even though it is possible that the experiments portrayed in these figure parts were performed under the same experimental conditions). The authors have been contacted by the Editorial Office to offer an explanation for the matter described above, although up to this time no response from them has been forthcoming. Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 42: 2839‑2848, 2018; DOI: 10.3892/ijmm.2018.3819].

Inflammatory bowel disease (IBD) pathogenesis reflects complex interactions between host immunity and gut microbiome dynamics, with microRNAs (miRNAs) functioning as key mediators of cross‑kingdom communication. Host‑derived miRNAs modulate bacterial gene expression and reshape microbial communities, while gut microbiota influences host miRNA expression through microbial metabolites and multiple immune signaling. In IBD, dysregulated miRNAs disrupt immune homeostasis by affecting inflammatory responses, lymphocyte differentiation and epithelial barrier integrity. Yet many miRNAs exhibit context‑dependent dual functions, complicating therapeutic targeting. Despite their biomarker potential for distinguishing IBD subtypes and tracking disease activity, clinical validation faces substantial obstacles including methodological inconsistencies, patient heterogeneity and temporal expression variability. Single-target miRNA therapeutics have yielded modest clinical outcomes, exposing the resilience of regulatory networks and compensatory mechanisms that limit intervention efficacy. The bidirectional architecture of miRNA‑microbiome communication argues against reductionist approaches. Effective IBD management requires integrated strategies that address multiple regulatory nodes rather than isolated pathways. Advancing this field demands deeper investigation of temporal dynamics, spatial organization and network‑level interactions. Such understanding will inform precision medicine strategies that restore regulatory equilibrium without compromising the adaptive capacity of host‑microbiome systems. Progress depends on recognizing the integrated nature of these regulatory networks rather than treating components in isolation.

X‑linked retinitis pigmentosa, primarily caused by mutations in the retinitis pigmentosa GTPase regulator (RPGR) gene, represents one of the most severe forms of inherited retinal degeneration, with early onset and rapid progression. Conventional interventions, such as vitamin A or docosahexaenoic acid supplementation, offer limited benefits and fail to halt disease progression. By contrast, gene therapy has emerged as a promising approach to alter the disease course. The present review summarizes the clinical phenotypes and pathogenic mechanisms associated with RPGR mutations, focusing on their disruption of ciliary transport and metabolic homeostasis. The present review further discusses advances in preclinical models, including mice, dogs, zebrafish and induced pluripotent stem cell‑derived organoids, that have facilitated the development of RPGR‑targeted therapies. Adeno‑associated virus‑based gene replacement has shown efficacy in restoring retinal structure and function, and several approaches have progressed to early‑phase clinical trials. Despite encouraging outcomes, challenges such as RPGR coding sequence instability, vector delivery efficiency and long‑term safety remain. The present review integrates current mechanistic understanding and therapeutic progress, providing a translational perspective for precision treatment of RPGR‑associated retinal diseases.