International journal of molecular medicine最新文献

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number of other articles that were written by different authors at different research institutes, several of which have been retracted, including one that had been published prior to the reciept of the above paper to International Journal of Molecular Medicine.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.

Musculoskeletal crosstalk is essential for maintaining the balance of bone metabolism, with macrophage‑derived exosomes emerging as key regulators of this process. Exosomes, small extracellular vesicles secreted by cells, carry a variety of bioactive molecules; proteins, lipids, mRNAs and miRNAs and facilitate intercellular communication by transferring these cargos to recipient cells. Specifically, macrophage‑derived exosomes mediate muscle‑bone interactions by transferring key regulators such as insulin‑like growth factor‑1 (IGF‑1) and fibroblast growth factor‑2 (FGF‑2), thereby playing a pivotal role in bone metabolic homeostasis. Macrophages are classified into pro‑inflammatory M1 and anti‑inflammatory M2 phenotypes, each performing distinct functions in immune responses. Exosomes from M1 macrophages typically carry pro‑inflammatory factors that can activate osteoclastic bone resorption, disrupting bone metabolism in pathological conditions. By contrast, exosomes from M2 macrophages often contain anti‑inflammatory factors that promote tissue repair and bone formation. In the context of bone metabolism, exosomes from M1 and M2 macrophages modulate muscle‑bone signaling by delivering regulators that influence the expression of IGF‑1 and FGF‑2, affecting osteoblast proliferation, differentiation, and mineralization. M1 macrophage‑derived exosomes activate signaling pathways such as NF‑κB and MAPK through the transfer of pro‑inflammatory cargo, thereby enhancing bone resorption. By contrast, exosomes from M2 macrophages can suppress pro‑inflammatory signaling while activating pathways like TGF‑β and PI3K/Akt, promoting bone synthesis and repair. As critical myokines, IGF‑1 and FGF‑2 not only support muscle growth, repair, and maintenance but also directly influence bone remodeling through musculoskeletal crosstalk.

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]

Mangiferin (MGF) is a natural C‑glucosyl xanthone with multitarget activity relevant to metabolic, inflammatory and cancer diseases. Notably, MGF modulates AMP‑activated protein kinase, NF‑κB, PI3K/AKT and MAPK signaling; through these pathways, it affects glucose and lipid metabolism, oxidative stress, apoptosis and inflammatory responses. In metabolic disorders, MGF has been shown to improve insulin sensitivity, support mitochondrial function and reduce diabetic complications. In cancer models, MGF suppresses proliferation, invasion and angiogenesis, and can influence antitumor immunity in the tumor microenvironment. Anti‑inflammatory actions include decreased cytokine release and regulation of the NLR family pyrin domain‑containing 3 inflammasome. Notably, clinical translation remains limited due to its low aqueous solubility, poor oral bioavailability and rapid metabolism. However, benefits of nanocarrier delivery, structural optimization and combination therapy have been reported, which may improve exposure and efficacy in experimental systems. Furthermore, safety signals in animals are favorable at relevant doses, but clinical evidence remains limited. In conclusion, the present review summarizes the pharmacodynamics and mechanisms of MGF across major disease settings and identifies key gaps for translation. Priorities include standardized clinical trials, optimization of delivery strategies, and rigorous assessment of long‑term safety and efficacy.

Ischemic heart disease remains the leading cause of global disease burden among cardiovascular disorders. In addition to cardiomyocyte injury, ischemia-reperfusion (I/R)-induced microvascular damage plays a crucial role in determining tissue dysfunction and overall prognosis. Mitochondria-associated endoplasmic reticulum membranes (MAMs), specialized contact sites between the ER and mitochondria, are now recognized as key regulators of cardiovascular pathophysiology. The present review summarized current knowledge of the structure of MAMs and their effects on endothelial cells under hypoxia/reoxygenation conditions. Particular attention was given to their role in regulating mitochondrial quality control processes, including fission, fusion, oxidative stress, mitophagy and Ca2+ homeostasis, within the context of cardiac microvascular I/R injury. Targeting MAMs may represent a promising strategy for microvascular protection in ischemic heart disease.

Atherosclerosis constitutes the fundamental pathological basis for cardiovascular diseases, with its pathogenesis intricately associated with dysfunctions in vascular endothelial and smooth muscle cells. Nanomaterials have emerged as a promising research focus within the biomedical field, attributed to their distinctive physicochemical properties. The present review explores the potential of nanomaterials, in conjunction with exercise interventions, to synergistically enhance vascular cell function, thereby presenting innovative therapeutic strategies against atherosclerosis. The present review systematically evaluates the various types of nanomaterials, elucidates their mechanisms of action, examines the synergistic effects of exercise interventions and discusses the challenges encountered in clinical translation, along with prospective directions for future research in this dynamic field.