Molecular medicine reports最新文献

Subsequently to the publication of this paper, and following the publication of an expression of concern statement (doi: 10.3892/mmr.2025.13679) that was published after an interested reader had noted that, regarding the confocal microscopic images shown in Fig. 3 on p. 2240, the top (Sham) and bottom (SCI) data panels appeared to show a small overlapping section such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source, the authors have now replied to the Editorial Office. After re‑examining their original data, the authors have realized that the data in Fig. 3 were inadvertently assembled incorrectly. The revised version of Fig. 3, now showing alternative data from one of the repeated experiments, is shown below. Note that this error did not significantly affect either the results or the conclusions reported in this paper, and all the authors agree with the publication of this corrigendum. Furthermore, the authors thank the Editor of Molecular Medicine Reports for granting them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [Molecular Medicine Reports 18: 2237‑2244, 2018; DOI: 10.3892/mmr.2018.9194].

Truncated‑cadherin (T‑cadherin) is a distinct glycosylphosphatidylinositol‑anchored atypical cadherin that differs from classical cadherins since it does not have transmembrane and intracellular domains. It primarily functions as a dual receptor, serving as a physiological receptor for low‑density lipoprotein (LDL) and a specific receptor for high‑molecular‑weight (HMW) adiponectin. Upon binding to LDL, T‑cadherin activates calcium signaling, thereby promoting cell proliferation and migration and contributing to the development of atherosclerotic plaques. Conversely, its interaction with HMW adiponectin mediates cardiovascular protective effects through various mechanisms, such as increased exosome secretion, reduced intracellular ceramide accumulation, improved insulin sensitivity and anti‑inflammatory actions. T‑cadherin is predominantly expressed in cardiovascular tissues, such as endothelial cells, smooth muscle cells, pericytes and cardiomyocytes. Genetic polymorphisms in cadherin‑13, the gene encoding T‑cadherin, are notably associated with the risk of hypertension, type 2 diabetes and end‑stage renal disease. In cancer, T‑cadherin generally has tumor‑suppressive effects, particularly in gastric, ovarian and breast cancers. This function is often compromised by promoter region hypermethylation, which leads to gene silencing and subsequently inhibits key signaling pathways, such as the PI3K/Akt, Wnt/β‑catenin and epithelial‑mesenchymal transition pathways. The present review provided a comprehensive overview of the molecular mechanisms, regulation of expression and potential clinical importance of T‑cadherin as a diagnostic biomarker and therapeutic target for cardiovascular diseases, including atherosclerosis, hypertension and heart failure, metabolic disorders, such as diabetes, and various cancers. Further research is required to fully elucidate the signal transduction pathways and competitive dynamics of T‑cadherin ligand binding.

Diffuse alveolar hemorrhage (DAH) is a rare life‑threatening pulmonary disorder in children, characterized by cough, hemoptysis and dyspnea. The pathogenesis is not fully understood, posing notable challenges for clinical diagnosis and management. Recent advances have gradually revealed potential etiologies and associated immune mechanisms, driving the development and application of novel therapies. The present review aimed to summarize the current understanding of the etiology, diagnostic approaches and therapeutic strategies for pediatric DAH, with a focus on the emerging role of the CD20 monoclonal antibody rituximab, and highlighted clinical evidence supporting its use in immune‑related DAH. The present review aimed to provide a foundation for further research and optimize clinical decision‑making.

Low back pain (LBP) is a leading cause of productivity loss worldwide and a major contributor to disability, imposing an economic burden on society. Intervertebral disc degeneration (IVDD) as a principal pathological driver of LBP remains a formidable therapeutic challenge, given that existing conservative and surgical interventions frequently fall short of achieving long‑term efficacy or halting disease progression. Advancements in molecular biology have revealed that circular RNAs (circRNAs) play a pivotal role in the intricate gene regulatory networks governing IVDD. The most extensively studied function of circRNAs is their ability to act as microRNA sponges. In addition, they participate in protein interactions, regulate gene transcription and serve as templates for protein translation. The present review provided a comprehensive overview of the current understanding of circRNA characteristics and functions, elucidated their involvement in IVDD pathogenesis and examined the therapeutic potential of emerging biomaterials for IVDD treatment. By consolidating existing research, the aim of this review was to offer theoretical foundations for innovative therapeutic strategies targeting IVDD.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the statistical analysis in this study may not have employed the most appropriate statistical tests; namely, the paired Student's t‑test was used for comparisons between independent groups, which the reader considered may have inflated the statistical significance. Neither may the paired Student's t‑test have been the most appropriate test to have been selected for various of the migration and invasion assay experiments, wherein at least three groups were being compared. Owing to the fact that the Editorial Office has been made aware of the possibility of inappropriate statistics handling in 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. [Molecular Medicine Reports 1: 641‑646, 2008; DOI: 10.3892/mmr_00000005].

The present study aimed to elucidate abnormal proliferation of colonic epithelial cells in type 2 diabetes mellitus (T2DM), a potential early step in colonic carcinoma development. Analysis of normal adjacent colonic epithelium obtained from colonic carcinoma surgeries showed an increased proliferative index among patients with T2DM. In vitro, high‑glucose medium mimicking diabetic conditions enhanced the proliferation of NCM460 cells, a normal human colon mucosal epithelial cell line. To identify dysregulated N6‑methyladenosine modifiers, the present study analyzed RNA sequencing datasets from the GEO database and identified an upregulated expression of insulin‑like growth factor 2 mRNA binding protein 2 (IGF2BP2) in the colonic epithelium of patients with T2DM, which was subsequently confirmed in the clinical samples and in vitro. IGF2BP2 knockdown inhibited the high glucose‑induced proliferation. Further bioinformatic evidence suggested midkine (MDK) as a potential target of IGF2BP2. MDK upregulation was confirmed in colonic epithelium under T2DM conditions, and its knockdown also inhibited high glucose‑induced proliferation. Overexpression of MDK partially prevented the anti‑proliferative effect of IGF2BP2 knockdown. Mechanistically, IGF2BP2 knockdown reduced MDK mRNA stability. RNA immunoprecipitation confirmed that IGF2BP2 bound to MDK mRNA, and this binding was significantly diminished upon mutation of the top three predicted N6‑methyladenosine modification sites in MDK. These findings suggested that the IGF2BP2/MDK axis contributed to abnormal colonic epithelial proliferation under T2DM conditions and may represent a potential therapeutic target to reduce carcinoma risk in patients with diabetes.

Cardiovascular diseases (CVDs) remain the primary cause of death worldwide. Exploring novel therapeutic targets is important for defining future research directions in cardiovascular medicine. Considering the notable role of cell death in disease pathogenesis, targeting disulfidptosis may represent a valuable therapeutic strategy for CVDs. However, current research increasingly centers on cancer, and the role of disulfidptosis in the cardiovascular field remains insufficiently explored. Accordingly, the present review examines the mechanisms of disulfidptosis across different cardiac cell types: Cardiomyocytes, vascular smooth muscle cells, endothelial cells and fibroblasts. Furthermore, the review discusses existing evidence for disulfidptosis in CVDs and potential intervention strategies, aiming to provide new perspectives for preventing and treating CVDs.

Urethral injury is a common type of traumatic damage to the urinary system, often leading to urethral stricture, fibrosis and dysfunction, which significantly impair physiological function and quality of life. The present study aimed to investigate the therapeutic efficacy of the novel immune‑regulatory molecule tetrahedral DNA nanostructure (TDN) in a rat model of urethral injury and explore the underlying mechanisms of action. A rat model of urethral injury was established through mechanical injury. Animals were divided into four groups: Control, model, model + rapamycin and model + TDN. Therapeutic effects and associated mechanisms were assessed via retrograde urethrography, Masson's trichrome staining, immunohistochemistry, western blotting, reverse transcription‑quantitative PCR (RT‑qPCR) and transcriptomic analysis. The results revealed that TDN markedly alleviated the immune response after urethral injury, reduced immune cell infiltration, downregulated the expression of inflammatory cytokines, including IL‑6, IL‑1β and TNF‑α, and effectively inhibited the progression of fibrosis. Masson's trichrome staining and western blotting provided evidence of reduced collagen deposition and decreased expression of fibrosis markers, including α‑smooth muscle actin, TGF‑β1, collagen I, collagen III and Smad3, after treatment with TDN. Transcriptomic analysis revealed that TDN modulated multiple immune‑related pathways, including the NF‑κB signaling pathway, NOD‑like receptor signaling pathway and cytokine‑cytokine receptor interaction, accompanied by a decrease in immune‑inflammatory responses, such as reduced inflammatory cytokine production and immune cell infiltration. Additionally, the results suggested that TDN may improve cellular metabolism and inhibit cell proliferation by downregulating the expression of cell cycle‑associated genes, as demonstrated by transcriptomic analysis and RT‑qPCR validation of cyclin B1, ribonucleotide reductase regulatory subunit M2, polo‑like kinase 1 and cyclin‑dependent kinase 1. In conclusion, TDN notably promoted tissue repair after urethral injury in rats by regulating the immune response, inhibiting fibrosis and enhancing cellular metabolism. These findings highlight TDN as a promising therapeutic candidate for urethral injury and offer novel insights into immune-regulatory strategies for the treatment of other fibrotic diseases.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data shown in Fig. 5A on p. 4978 were strikingly similar to data that had either appeared previously in other papers written by different authors at different research institutes, or which had already been submitted for publication. In view of the fact that the abovementioned data had already apparently been published prior to its submission to Molecular Medicine Reports, the Editor 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. [Molecular Medicine Reports 20: 4973‑4983, 2019; DOI: 10.3892/mmr.2019.10737].

Tubulointerstitial injury is a key driver of lupus nephritis (LN) progression, and dysregulation of the immune microenvironment is a central feature of this process. The molecular mediators of this dysregulation remain incompletely defined. In the present study an integrated bioinformatics and experimental analysis was performed of the Activator Protein 1 (AP‑1) family transcription factor Fos‑related antigen 1 (FRA1) in LN tubulointerstitium. Analysis of gene expression omnibus datasets (GSE113342, GSE200306 and GSE127797) showed that FRA1 was markedly upregulated in the tubulointerstitium of LN samples and that its expression positively correlated with CD8⁺ T cells, regulatory T cells, monocytes, M1 macrophages and activated mast cells, but negatively correlated with plasma cells, resting CD4⁺ memory T cells, M0/M2 macrophages, resting dendritic cells and resting mast cells. In vivo experiments revealed that, FRA1 expression was also increased in kidneys from MRL/lpr mice. Furthermore, in vitro, lentiviral overexpression of FRA1 in HK‑2 cells induced robust upregulation of IL‑6, IL‑1β, IL‑8, MCP‑1 and RANTES, whereas FRA1 knockdown selectively decreased IL‑6 and RANTES levels. Together, these results indicate that FRA1 is significantly elevated in the LN tubulointerstitium and may foster a proinflammatory microenvironment by regulating key cytokines. The FRA1/AP‑1 axis therefore represents a potential regulator of renal inflammation in LN and a candidate therapeutic target.