International journal of molecular medicine最新文献

Following the publication of this paper, it was drawn to the Editor's attention by an interested reader that, regarding the immunohistochemical images in Fig. 2A on p  809, the Control/SG and UA/SG data panels contained an overlapping data section, suggesting that these data panels had been derived from the same original source. In addition, concerning the outer hair cell images shown in Fig. 4A on p. 811, the CDDP/TRITC and UA+CDDP/TRITC data panels appeared to be matching, suggesting that this figure had also been assembled incorrectly. Upon contacting the authors about these issues, they realized that Figs. 2 and 4 in this paper had inadvertently been assembled incorrectly. The revised versions of Figs. 2 and 4, now featuring the correct data for the UA/SG panel in Fig. 2A and the CDDP/TRITC data panel in Fig. 4A, are shown 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 46: 806‑816, 2020; DOI: 10.3892/ijmm.2020.4633].

Following the publication of the above paper, a concerned reader has drawn to the Editor's attention that the data shown for the p-AMPKα blots with the RT-qPCR analysis in Fig. 2B on p. 203 are strikingly similar to the ATG7 blots shown in Fig. 4A on p. 205. The authors were contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in this paper, although up to this time, no response from the authors 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 39: 199-207, 2017; DOI: 10.3892/ijmm.2016.2824].

Claudin‑7 (CLDN7) is a key component of epithelial tight junctions. It plays a vital role in maintaining cell polarity, barrier integrity and paracellular transport. Abnormal CLDN7 expression is closely related to the onset and progression of various diseases. It is especially markedly associated with the growth and metastasis of multiple cancers. Additionally, dysregulated CLDN7 expression contributes to the progression of intestinal, skin and respiratory system diseases. The present review summarized the structure, expression, physiological functions, stability and regulatory mechanisms of CLDN7, emphasizing its role in tumors. The expression patterns, regulatory mechanisms, effect on malignant phenotypes and clinical significance of CLDN7 were also discussed.

Pemphigus vulgaris (PV) is a life‑threatening autoimmune blistering disease characterized by acantholysis (the loss of cell‑cell adhesion of keratinocytes) and the formation of non‑healing suprabasal intraepidermal blisters. The progression of keratinocyte acantholysis in PV is complex. Interleukin‑37 (IL‑37), which functions through receptor binding, exerts a protective role in PV. However, the specific receptor mediating the effect of IL‑37 in PV and the underlying mechanisms remain unclear. The present study found elevated levels of IL‑37, a natural suppressor of innate inflammatory and immune responses, in patients with PV. IL‑37 treatment directly suppressed both acantholysis and apoptosis in keratinocytes. Mechanistic investigations using co‑immunoprecipitation revealed that IL‑37 binds to interleukin‑1 receptor 8 (IL‑1R8). Knockdown of IL‑1R8 (or IL‑18Rα) abolished the inhibitory effects of IL‑37 on acantholysis and apoptosis. Furthermore, the IL‑37/IL‑1R8 complex suppressed epidermal growth factor receptor (EGFR) signaling, and reduced the expression of TNF‑alpha‑converting enzyme (ADAM17). Activation of EGFR using specific agonists reversed the IL‑37‑mediated reduction in acantholysis and apoptosis in HaCaT cells. In conclusion, IL‑37 treatment markedly attenuated keratinocyte dissociation and apoptosis in PV through the IL‑1R8/ADAM17/EGFR pathway. These findings provide novel mechanistic insights into the immunoregulatory functions of IL‑37.

Neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis, are characterized by progressive loss of neurons. Although the precise pathogenesis of such diseases is complex and multifactorial, several molecular pathways have been implicated, including the aggregation of misfolded proteins, mitochondrial dysfunction, oxidative stress, neuroinflammation and disrupted iron homeostasis. Emerging evidence has underscored the pivotal role of ferroptosis, an iron‑dependent, non‑apoptotic form of cell death, in neurodegenerative disease progression. Ferritin, characterized by a 24‑subunit hollow sphere structure composed of heavy and light chains, plays a key role in the network regulating cerebral iron homeostasis. In response to cellular iron overload, ferritin expression is upregulated to sequester labile iron and mitigate Fenton reaction‑mediated toxicity, thus exerting a cytoprotective function. Paradoxically, ferritin can be degraded via ferritinophagy, a selective autophagic process that releases toxic ferrous iron and directly triggers ferroptosis. This review systematically reviews the role of ferritin within the iron homeostasis network to elucidate the connection between the dysregulation of iron metabolism and the pathological mechanisms of neurodegenerative diseases. The study focused on the potential role of ferritin as a biomarker for early diagnosis, therapeutic strategies targeting ferritin pathways to restore iron homeostasis and the clinical translational value of magnetic resonance imaging‑based non‑invasive quantification of cerebral iron deposition. It is crucial to elucidate the multidimensional roles of ferritin in neurodegeneration to provide a theoretical foundation for precision diagnostic and therapeutic approaches.

Fetal growth restriction (FGR) is strongly associated with adverse perinatal outcomes, and placental oxidative stress has been identified as a central pathological mechanism. In maternal plasma, cord blood and placental tissues from FGR pregnancies, the levels of malondialdehyde, 4‑hydroxynonenal, reactive oxygen metabolites and 8‑hydroxy‑2'‑deoxyguanosine are consistently elevated. In parallel, superoxide dismutase and glutathione peroxidase show compensatory upregulation, while catalase activity declines, reflecting increased oxidative burden coupled with impaired antioxidant defense. Major sources of reactive oxygen species include NADPH oxidase and xanthine oxidase, mitochondrial electron transport and ischemia‑reperfusion events. Mechanistic evidence further indicates that oxidative stress interacts with endoplasmic reticulum stress, metabolic reprogramming and epigenetic alterations, thereby aggravating trophoblast dysfunction and placental vascular injury. Aberrant DNA hypomethylation, histone modifications and dysregulation of noncoding RNAs, such as microRNA (miR)‑199a, miR‑210‑3p and miR‑21, contribute to persistent remodeling of trophoblast behavior and vascular networks. Early clinical studies have suggested that melatonin and pentoxifylline may alleviate placental oxidative injury and improve selected perinatal outcomes, whereas vitamin C and E supplementation shows no clear benefit. Preclinical investigations have highlighted the potential of mitochondria‑targeted and classical antioxidants, including mitoquinone mesylate, N‑acetylcysteine, tempol and resveratrol; however, their efficacy and safety appear to be dependent on gestational timing and dosage. Further well-designed clinical trials are warranted to establish effective antioxidant‑based strategies for FGR.

Following the publication of the above paper, a concerned reader has drawn the Editor's attention to the fact that, regarding the western blot data shown in Fig. 4A and E on p. 612, the p‑p38 blots featured in these figure parts were strikingly similar, although the blots were rotated through 180° relative to each other. Upon investigating the data in this paper independently in the Editorial Office, it also came to light that β‑actin control blots featured in Fig. 1E, and p‑p38 blots featured in Fig. 5I, subsequently appeared in another paper written by the same research group in an article published in the journal PLoS One. Finally, control western blots appeared to have been re‑used in Fig. 4A and C, although the experimental conditions reported for the western blots in these figure parts were different. The authors have been contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in this paper, and we are awaiting their response. 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 these potential problems while the Editorial Office continues to investigate this matter further.  [International Journal of Molecular Medicine 27: 607‑615, 2011; DOI: 10.3892/ijmm.2011.621].

Excessive inflammation and scar formation at the tendon‑bone interface (TBI) hinder effective healing. Macrophage efferocytosis is critical for resolving inflammation, yet its regulatory mechanisms in TBI healing remain unclear. The present study investigated the role of zinc finger E‑box binding homeobox 1 (ZEB1) in macrophage efferocytosis and rotator cuff repair. Zeb1 knockdown in rats was achieved using short hairpin RNA (shRNA). Bone marrow‑derived macrophages co‑cultured with apoptotic Jurkat cells were used to evaluate efferocytosis efficiency. Mechanistically, ZEB1 was demonstrated to function as a critical regulator of mitochondrial dynamics by transcriptionally repressing Mitofusin‑2 (MFN2), thereby maintaining the mitochondrial fission necessary for efficient efferocytosis. ZEB1‑knockdown relieved MFN2 suppression, leading to excessive mitochondrial fusion and a subsequent decrease in apoptotic cell clearance. In vivo, ZEB1 deficiency resulted in the accumulation of secondary necrotic cells, aggravated the inflammatory microenvironment (increased M1/decreased M2 polarization), and impaired histological and biomechanical healing of the tendon‑bone interface. These findings indicate a novel ZEB1/MFN2/mitochondrial fission axis that governs macrophage efferocytosis. Targeting this axis to restore the immune microenvironment offers a potential therapeutic strategy for improving tendon‑bone healing.

Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 2D on p. 834 showing the results of Transwell cell migration assay experiments for the U‑2OS cell line, the 'U‑2OS 24 h/Control' and 'U‑2OS 24 h/AST‑IV' data panels contained an overlapping section, such that these data panels were apparently derived from the same original source, where the results of differently performed experiments were intended to have been portrayed. Upon performing an independent analysis of the data in this paper in the Editorial Office, it also came to light that two pairs of data panels comparing Figs. 2C and 4C, and 2D and 4D, also contained overlapping sections. After having consulted their original data, the authors realized that Fig. 2 had inadvertently been assembled incorrectly. The revised version of Fig. 2, now showing the correct data for the 'MG‑64 48 h/AST‑IV', U‑2OS 24 h/AST‑IV' and 'U‑2OS 48 h/AST‑IV' panels in Fig. 2C and D, is shown on the next page. The authors can confirm that the errors associated with this figure did not have any 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 43: 830‑838, 2019; DOI: 10.3892/ijmm.2018.4013].

Abdominal aortic aneurysm (AAA) is a fatal cardiovascular disease with no effective drug treatment currently available. The aberrant expression levels of microRNAs (miRNAs or miRs) contribute to AAA pathogenesis. In the present study, miRNA microarray analysis was performed to screen for differentially expressed miRNAs in the aortas of AAA mice compared with those in control mice, and to clarify the role and mechanism of miRNA‑378a‑5p (miR‑378a‑5p) in the AAA development. A comprehensive miRNA microarray analysis was conducted to screen for differentially expressed miRNAs in the aortas of AAA mice and control mice. Reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) was used to detect the expression levels of miR‑378a‑5p in the serum and aortas of patients with AAA and mice. To clarify the role of miR‑378a‑5p in the AAA development in vivo, miR‑378a‑5p antagomir and angomir were administered to ApoE‑/‑ mice using tail venous injection, followed by Angiotensin II (Ang II) infusion. Next, the role of miR‑378a‑5p in the phenotypic switching and migration of vascular smooth muscle cells (VSMCs) was examined in vivo and in vitro. Mechanistically, the targets of miR‑378a‑5p were identified by bioinformatics analysis, luciferase assay, RT‑qPCR and western blotting. Co‑immunoprecipitation assay combined with mass spectrometry were carried out for excavating potential downstream effectors. The expression of miR‑378a‑5p was decreased in the serum and aortas of patients with AAA (aortic dissection) and mice, and tumor necrosis factor‑α‑treated VSMCs. In vivo, the antagomir‑378a‑5p aggravated AAA formation, as evidenced by a larger maximal aortic diameter and greater medial elastin degradation than in control mice. miR‑378a‑5p angomir had the opposite effect. In vitro, miR‑378a‑5p overexpression significantly promoted the contraction ability and suppressed the migration of VSMCs, whereas miR‑378a‑5p knockdown inhibited the contraction ability and increased the migration of VSMCs. Mechanistically, it was identified that miR‑378a‑5p played a protective role in AAA development by regulating actin‑binding LIM protein 1 (ABLIM1)‑megakaryoblastic leukemia 1 (MKL1) pathway. miR‑378a‑5p exerts protective effects against AAA by maintaining VSMCs homeostasis via the ABLIM1‑MKL1 pathway. Therefore, targeting miR‑378a‑5p may be an attractive therapeutic strategy for AAA treatment.