International journal of molecular medicine最新文献

Adrenic acid is a 22‑carbon unsaturated fatty acid that is widely present in the adrenal gland, liver, brain, kidney and vascular system that plays a regulatory role in various pathophysiological processes, such as inflammatory reactions, lipid metabolism, oxidative stress, vascular function, and cell death. Adrenic acid is a potential biomarker for various ailments, including metabolic, neurodegenerative and cardiovascular diseases and cancer. In addition, adrenic acid is influenced by the pharmacological properties of several natural products, such as astragaloside IV, evodiamine, quercetin, kaempferol, Berberine‑baicalin and prebiotics, so it is a promising new target for clinical treatment and drug development. However, the molecular mechanisms by which adrenic acid exerts are unclear. The present study systematically reviewed the biosynthesis and metabolism of adrenic acid, focusing on intrinsic mechanisms that influence the progression of metabolic, cardiovascular and neurological disease. These mechanisms regulate several key processes, including immuno‑inflammatory response, oxidative stress, vascular function and cell death. In addition, the present study explored the potential clinical translational value of adrenic acid as a biomarker and therapeutic target. To the best of our knowledge, the present study is first systematic summary of the mechanisms of action of adrenic acid across a range of diseases. The present study provides understanding of the wide range of metabolic activities of adrenic acid and a basis for further exploring the pathogenesis and therapeutic targets of various diseases.

DNA methylation is one of the earliest discovered and most extensively studied epigenetic regulatory mechanisms. Broadly, DNA methylation refers to the transfer of a methyl group on S‑adenosine‑L‑methionine (SAM) to the C5 site of cytosine, a reaction catalysed by DNA methyltransferase (DNMT). This process can either up‑ or down‑regulate gene expression due to gene promoter methylation, leading to the occurrence of certain diseases. Urinary system diseases, known for their high prevalence and complex pathogenesis, significantly affect the lives and health of patients. Urological tumours, in particular, represent a non‑negligible disease burden worldwide. With the development of epigenetics, an increasing number of studies have demonstrated that DNMT plays an important role in urinary system disease. The present review aims to explore the relationship between DNMT and urinary system diseases and the potential of DNMT in the clinical management of these diseases.

N6‑methyladenosine (m⁶A) is one of the most universal, abundant and conserved types of internal post‑transcriptional modifications in eukaryotic RNA, and is involved in nuclear RNA export, RNA splicing, mRNA stability, gene expression, microRNA biogenesis and long non‑coding RNA metabolism. AlkB homologue 5 (ALKBH5) acts as a m6A demethylase to regulate a wide variety of biological processes closely associated with tumour progression, tumour metastasis, tumour immunity and tumour drug resistance. ALKBH5 serves a crucial role in human digestive system tumours, mainly through post‑transcriptional regulation of m⁶A modification. The present review discusses progress in the study of the m6A demethylase ALKBH5 in gastrointestinal tract cancer, summarizes the potential molecular mechanisms of ALKBH5 dysregulation in gastrointestinal tract cancer, and discusses the significance of ALKBH5‑targeted therapy, which may provide novel ideas for future clinical prognosis prediction, biomarker identification and precise treatment.

Traditional Chinese Medicine (TCM) has demonstrated promising efficacy in managing and preventing the early‑stage diabetic nephropathy (DN). Although the exact mechanisms remain elusive, clinical evidence has suggested that Jinlida granules (JLD) are beneficial in improving renal function among patients with DN. The present study aimed to elucidate the effect of JLD on DN and the underlying molecular mechanism. Therefore, podocyte apoptosis was evaluated using flow cytometry and TUNEL staining, while mitochondrial morphology and function were assessed using transmission electron microscopy, MitoTracker, JC‑1 and reactive oxygen species staining. RNA sequencing analysis was performed to elucidate the mechanism underlying the effect of JLD on DN. Additionally, to investigate the role of peroxisome proliferator‑activated receptor‑γ co‑activator‑1α (PGC‑1α) in mitigating JLD‑induced mitochondrial dysfunction and podocyte apoptosis, MPC5 cells were transfected with the corresponding small interfering RNA constructs. The results showed that JLD effectively improved renal function and mitigated podocyte injury, as well as ameliorated mitochondrial dysfunction and inhibited apoptosis in db/db mice. In vitro experiments further revealed that JLD exerted a protective effect via inhibiting mitochondrial fission and apoptosis in high glucose‑treated podocytes. Furthermore, JLD enhanced the phosphorylation of adenosine monophosphate‑activated protein kinase (AMPK), thus promoting the expression of PGC‑1α, eventually improving apoptosis and mitochondrial homeostasis. Overall, the current study revealed that JLD could improve mitochondrial homeostasis and reduce cell apoptosis in podocytes via activating the AMPK/PGC‑1α pathway, thus providing a theoretical foundation for the clinical management of DN.

Following the publication of this article, a concerned reader drew to the Editor's attention that, in the tumor tissue images shown in Fig. 5A and B on p. 1001, there were two pairs of overlapping data panels, such that data which were intended to show the results from differently performed experiments appeared to have been derived from the same original sources. Subsequently, after having conducted a separate investigation in the Editorial Office, it came to light that there were also matching data panels intending to show the results from different experiments in the flow cytometric plots shown in Fig. 2; moreover, there appeared to be potential issues with the presentation of some of the western blots in Fig. 3.  Although the possibility of a corrigendum was considered, upon reflection, the Editor of International Journal of Molecular Medicine has decided that, owing to the number of problems that were identified with the data in the published paper, the article should be retracted from the publication on account of data mishandling issues and 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 reply. The Editor apologizes to the readership for any inconvenience caused, and thanks the interested reader for initially drawing this matter to our attention.[International Journal of Molecular Medicine 35: 995‑1002, 2015; DOI: 10.3892/ijmm.2015.2096].

Solute carrier (SLC) transporters are involved in various biological processes associated with metabolic reprogramming and cancer, supporting the increased requirement of nutrients and energy. Over the past decade, there have been significant advancements in understanding the expression and function of SLCs in ovarian cancer (OC). This gynecological condition has a high mortality rate and limited treatment options; thus, early diagnosis remains a target clinically. OC exhibits complexity and heterogeneity, resulting in different clinical characteristics, resistance to chemotherapy drugs and poor prognosis. Additionally, SLCs have a different expression pattern between healthy and tumor tissue, and consequently, their inhibition or activation could modify signaling pathways involved in the tumor growth process, such as cell proliferation, apoptosis and drug accumulation. The present review aims to consolidate current data to provide a comprehensive understanding of the potential importance of SLCs in OC. Additionally, it seeks to offer guidance for further research on utilizing SLCs as prognostic biomarkers and therapeutic targets.

Bone marrow mesenchymal stem cells (MSCs) serve a pivotal role in the hematopoietic niche. The present study collected bone marrow samples from individuals across various age groups to investigate the biological characteristics of MSCs. By modifying the bone marrow microenvironment through co‑culture techniques, changes in the stemness of MSCs were examined. An in vitro hematopoietic co‑culture system was established to simulate the impact of MSCs on hematopoietic stem cells. The results demonstrated that the mode of cell‑to‑cell contact among stem cells is more influential in shaping bone marrow function compared with the effects of aging on these stem cells. Transcriptomic analysis revealed that MSCs serve as essential mediators, with their growth variations being both a consequence and a cause of changes in the bone marrow microenvironment. Furthermore, the decline in hematopoietic function observed in the elderly is a manifestation of this phenomenon. Data from the present study suggest that targeting MSCs is essential for enhancing bone marrow function and improving the outcomes of bone marrow transplantation.

Following the publication of the above article, the authors contacted the Editorial Office to explain that three pairs of the western blots featured in Fig. 4 on p. 165 had inadvertently been duplicated in this figure. Essentially, it appeared to the authors that the blots in Fig. 4A for SIRT5 were identical to those in Fig. 4C for SIRT6 (P2 versus C2); the blots in Fig. 4B for SIRT4 were identical to those in the same figure part for SIRT5; and the blots in Fig. 4C for SIRT6 (P3 versus C3) were identical to those in Fig. 4C for SIRT7 (P1 versus C1). The authors were able to re‑examine their original data, and identified the data that should have rightfully been included in this figure. The revised version of Fig. 4, now incorporating the correct data for SIRT6 (P2 versus C2) in Fig. 4C, SIRT5 in Fig. 4B, and SIRT7 (P1 versus C1) in Fig. 4C, is shown on the next page. The authors can confirm that the errors associated with this figure 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 44: 157‑171, 2019; DOI: 10.3892/ijmm.2019.4173].

Inflammatory bowel diseases (IBDs), which encompasses Crohn's disease and ulcerative colitis, is a chronic inflammatory condition associated with an increased risk of colorectal cancer (CRC). Small RNAs have been linked to various illnesses, including IBD and CRC. These small RNAs also serve as potential biomarkers for these diseases, offering a cutting‑edge approach to investigating possible treatments. To date, treatments involving oral nucleic acid usage are still unachievable due to the instability of medications in the gastrointestinal tract (GIT), their lack of ability to effectively target disease tissues and their notable adverse effects. However, nanoparticle or exosome delivery systems of nucleic acid medications effectively target disease tissues by overcoming the instability of the GIT, resulting in an effective outcome. In the present review, the biogenesis of small RNAs (tRNA‑derived small RNA, microRNA, small nucleolar RNA and p‑element‑induced wimpy testis‑interacting RNA), their roles in the pathogenesis of IBD and CRC as well as their application as possible diagnostic and prognostic biomarkers in IBD and CRC are discussed.