International journal of molecular medicine最新文献

Following the publication of the above article, a concerned reader drew the Editor's attention to the fact that the figures presented in this paper appeared to contain the following anomalies: In Fig. 4D, the 'Met 5 mM' and 'Met 10 mM' data panels were overlapping; in Fig. 8F, the 'IF116 si' and 'IF116 si + Met' data panels were overlapping; in Fig 5A, the 'Un' and 'Ctr' rows of data were overlapping; and in Fig. 7A, the 'Ctr' and 'IF116 Si' rows of data were overlapping. In addition, after having performed an independent analysis of the data in this paper in the Editorial office, it came to light that the 'Met 0 mM' panel in Fig. 4D contained an overlapping section with the Control panel in Fig. 8F. Given that these issues have come to light, the Editor of International Journal of Molecular Medicine has decided that this article should be retracted from the publication on the grounds of an overall 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 satisfactory reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 41: 1365‑1376, 2018; DOI: 10.3892/ijmm.2017.3346].

The apelin/elabela‑apelin receptor (APJ) signaling system is a key regulator of metabolic homeostasis and cardiovascular function in diabetes mellitus. However, its therapeutic application is complicated by its functional divergence: the system exerts protective effects in some tissues while driving pathology in others. The present review examined these distinct roles, focusing on how the biological outcome depends on the specific ligand, disease stage and tissue microenvironment. It discussed the molecular mechanisms underlying this divergence, as well as the varying roles of the same receptor at different stages of the same disease. Finally, it evaluated emerging therapeutic strategies, such as stabilized analogs and biased agonists, proposing that precise targeting of the APJ conformational landscape offers a pathway to move beyond glycemic control toward multi‑organ protection in diabetes.

Cardiovascular diseases remain the leading cause of global morbidity and mortality, imposing a significant burden on families and societies. E26 transformation‑specific (ETS)‑1 and ETS‑2, members of the ETS family of transcription factors (also known as proto‑oncogenes), are increasingly recognized for their roles in tumor progression. Recent studies highlight their importance in normal coronary artery development, myocardial homeostasis and the regulation of vascular inflammation and remodeling. Emerging evidence suggests that ETS‑1/ETS‑2 are critical in the pathogenesis of atherosclerosis, myocardial ischemia‑reperfusion injury, cardiac remodeling and heart failure. The present review summarized the research progress of ETS‑1/ETS‑2 in cardiovascular diseases, discusses the relevant challenges encountered in the translational process of ETS‑1/ETS‑2‑targeted therapy for cardiovascular diseases and provides novel strategies for the treatment of cardiovascular diseases targeting ETS‑1/ETS‑2.

Following the publication of the above article, an interested reader drew to the authors' attention that, concerning the images showing the construction of the CX3CL1‑over-expression adenovirus and the CX3CL1 short hairpin RNA (shRNA) adenovirus in Fig. 1 on p. 1581, the 'P3x100, Ad‑CX3CL1 OE' data panel in Fig. 1A contained an overlapping section with the 'P3x100, Ad‑CX3CL1 shRNA1' data panel in Fig. 1B, such that these were apparently derived from the same original source where different experiment conditions were reported. In addition, for the lung pathology images shown in Fig. 3 on p. 1584, the images showing the 'ASPx100' and the 'M+Ax100' experiments were apparently identical, suggesting that this figure had also been assembled incorrectly. After re‑examining their original data, the authors regret that Figs. 1 and 3 did contain errors in terms of their assembly, as identified by the external reader. Concerning Fig. 1, the authors wish to point out that these experiments were performed by the virus packaging company (Hanbio Biotechnology), who acknowledged that they were responsible for the error that was made in the provision of the images for this figure. Moreover, this error did not have any real significance in terms of the reported reports in this study, since neither shRNA1 nor shRNA2 was ultimately selected as the vector for the subsequent experiments; shRNA3 was selected as the interference vector of choice. Therefore, the Editor has approved the inclusion of a new version of Fig. 1 in this Corrigendum, comprising only the data for shRNA3 in Fig. 1B.Regarding Fig. 3, the revised version of this is also shown in the subsequent pages, showing the correct data for the 'Nx100', 'ASPx100' and 'M+Ax100' panels. Note that the revisions made to these figures do not affect the overall conclusions reported in the paper. The authors express their gratitude to the Editor of International Journal of Molecular Medicine for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 39: 1580‑1588, 2017; DOI: 10.3892/ijmm.2017.2969].

Pyroptosis is a lytic and highly inflammatory type of programmed cell death that is mediated primarily by members of the gasdermin (GSDM) protein family. Upon activation by inflammatory stimuli or danger signals, GSDMs are cleaved to release N‑terminal fragments that oligomerize and form pores in the plasma membrane. This disrupts cellular integrity, resulting in osmotic lysis and the release of potent proinflammatory cytokines, such as interleukin (IL)‑1β and IL‑18. The progression of an aortic aneurysm (AA) is driven by complex pathophysiological processes, with the loss of vascular smooth muscle cells and sustained vascular inflammation being central to disease pathogenesis. Emerging evidence indicates that pyroptosis markedly contributes to AA development by amplifying inflammatory activation and promoting cellular disintegration within the aortic wall. Further preclinical evidence has demonstrated that pharmacological inhibition of key pyroptosis signaling pathways effectively attenuates AA formation in murine models, underscoring its promising therapeutic potential. The present review summarizes the molecular mechanisms of pyroptosis, highlights its pathophysiological role in AAs and discusses novel therapeutic strategies targeting pyroptosis for the treatment of AAs.

Diabetic kidney disease (DKD), a predominant contributor to end‑stage renal disease, is distinguished by its intricate pathogenesis and constrained therapeutic interventions. The present review discusses the role of glycolytic flux‑mediated protein lactylation, an emerging epigenetic modification, in the progression of DKD. Under conditions of hyperglycemia and hypoxia, renal cells undergo a metabolic shift towards glycolysis, resulting in the accumulation of lactate. Beyond its role as a metabolic byproduct, lactate functions as a signaling molecule that facilitates the lactylation of both histones and non‑histone proteins. The present review discusses how lactylation has been implicated in key pathological mechanisms in DKD, including ferroptosis, dysregulated autophagy and fibrosis. The interplay between lactylation and other posttranslational modifications is also discussed, along with the therapeutic potential of targeting the glycolysis‑lactylation axis. By highlighting this metabolic‑epigenetic crosstalk, the present review proposes a conceptual framework that may inform the development of diagnostic and therapeutic strategies targeting lactylation in DKD.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data featured in Figs. 2 and 5, and the control western blot data in Fig. 6A were strikingly similar to data which had been already been submitted for publication in articles that were written by different authors at different research institutes. Owing to the fact that the contentious flow cytometric and western blot data in the above article were found to be strikingly similar to data that had already been submitted for publication 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 38: 1507‑1514, 2016; DOI: 10.3892/ijmm.2016.2755].

Sepsis is a life‑threatening syndrome of organ dysfunction caused by infection, characterized by complex pathogenesis and high clinical mortality. As innate immune cells, macrophages serve a pivotal role in the initiation, progression and resolution of sepsis. The present review focuses on the key molecular nodes and signaling pathways of macrophage metabolic reprogramming in the process of sepsis. Key mechanisms include: i) The mammalian target of rapamycin‑hypoxia inducible factor‑1α (HIF‑1α)‑pyruvate kinase M2 axis as the primary regulator of glycolytic flux and pro‑inflammatory cytokine production; ii) tricarboxylic acid cycle interruption leading to succinate accumulation, which amplifies HIF‑1a signaling and promotes interleukin‑1β release via G protein‑coupled receptor 91, thereby exacerbating inflammation; iii) triggering receptor expressed on myeloid cells 2‑SH2‑containing protein tyrosine phosphatase‑1 axis‑mediated impairment of fatty acid oxidation, promoting lipid accumulation and pro‑inflammatory activation; and iv) amino acid depletion contributing to immune paralysis. In view of the 31.5% global mortality (21.4 million mortalities in 2021) caused by sepsis, a shift from supportive treatment to precise immune metabolism intervention is needed. The present article uniquely integrates the coordinated regulation of glucose, lipid and amino acid metabolic networks of macrophages in sepsis, and expounds the research status of immune metabolism in sepsis, in order to provide reference for the clinical treatment of sepsis. Targeted modulation of macrophage metabolism offers a new direction for individualized immunometabolic therapy in sepsis.

DNA damage and repair mechanisms are crucial for maintaining genomic stability, and their dysregulation is closely linked to the complex pathogenesis of autoimmune diseases. The present review systematically describes the types of DNA damage, key repair pathways, their regulatory networks, and the multidimensional interactions between DNA repair and the immune system. Furthermore, it delves into how defective DNA repair drives the development of autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis through mechanisms encompassing cyclic GMP‑AMP synthase (cGAS)‑stimulator of interferon genes (STING) pathway activation, self‑antigen release and breakdown of immune tolerance. Oxidative stress‑induced DNA damage, mutations in repair genes and aberrant accumulation of cytosolic DNA are key triggers of autoimmune responses. In addition, DNA repair proteins indirectly influence disease progression by modulating immune cell functions, including T‑cell homeostasis and macrophage polarization. The present review further summarizes the therapeutic potential and challenges of targeting DNA damage response pathways, including via poly adenosine diphosphate ribose polymerase inhibitors and cGAS‑STING axis regulation, as demonstrated in pre‑clinical models. Future research leveraging multi‑omics and innovative delivery systems will be crucial for translating these discoveries into effective, personalized therapies. The present review advances the development of personalized precision medicine and provides a solid theoretical foundation for developing novel treatment strategies.

Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the photomicrographs shown in Fig. 1 on p. 195, the 'I/R' and 'Control' data panels (for the Day 1 experiments) contained an overlapping section, such that data which were intended to show the results of differently performed experiments were apparently derived from the same original source. The authors have been contacted by the Editorial Office to offer an explanation for the apparent anomaly in the presentation of the data in their 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 this potential problem while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 28: 193‑198, 2011; DOI: 10.3892/ijmm.2011.659].