The Best Exercise Modality and Dose to Reduce Glycosylated Hemoglobin in Patients with Type 2 Diabetes: A Systematic Review with Pairwise, Network, and Dose-Response Meta-Analyses.

Background: Persistently elevated glycosylated hemoglobin (HbA1c) is associated with a higher risk of long-term vascular complications.

Objective: We evaluated the effect of different exercise modalities and doses on HbA1c levels in patients with type 2 diabetes.

Methods: A systematic search for randomized controlled trials involving exercise interventions in patients with type 2 diabetes was conducted across seven electronic databases, encompassing data from their inception up to October 2023.

Fructose-1,6-bisphosphatase 1 dephosphorylates and inhibits TERT for tumor suppression.

Telomere dysfunction is intricately linked to the aging process and stands out as a prominent cancer hallmark. Here we demonstrate that telomerase activity is differentially regulated in cancer and normal cells depending on the expression status of fructose-1,6-bisphosphatase 1 (FBP1). In FBP1-expressing cells, FBP1 directly interacts with and dephosphorylates telomerase reverse transcriptase (TERT) at Ser227.

Application of deep learning in radiation therapy for cancer.

In recent years, with the development of artificial intelligence, deep learning has been gradually applied to clinical treatment and research. It has also found its way into the applications in radiotherapy, a crucial method for cancer treatment. This study summarizes the commonly used and latest deep learning algorithms (including transformer, and diffusion models), introduces the workflow of different radiotherapy, and illustrates the application of different algorithms in different radiotherapy modules, as well as the defects and challenges of deep learning in the field of radiotherapy, so as to provide some help for the development of automatic radiotherapy for cancer.

5-Hydroxytryptophan acts as a gap junction inhibitor to limit the spread of chemotherapy-induced cardiomyocyte injury and mitochondrial dysfunction.

Anthracycline chemotherapeutics like doxorubicin (DOX) are widely used against various cancers but are accompanied by severe cardiotoxic effects that can lead to heart failure. Through whole transcriptome sequencing and pathological tissue analysis in a murine model, our study has revealed that DOX impairs collagen expression in the early phase, causing extracellular matrix anomalies that weaken the mechanical integrity of the heart. This results in ventricular wall thinning and dilation, exacerbating cardiac dysfunction.

The interplay of the circadian clock and metabolic tumorigenesis.

The circadian clock and cell metabolism are both dysregulated in cancer cells through intrinsic cell-autonomous mechanisms and external influences from the tumor microenvironment. The intricate interplay between the circadian clock and cancer cell metabolism exerts control over various metabolic processes, including aerobic glycolysis, de novo nucleotide synthesis, glutamine and protein metabolism, lipid metabolism, mitochondrial metabolism, and redox homeostasis in cancer cells. Importantly, oncogenic signaling can confer a moonlighting function on core clock genes, effectively reshaping cellular metabolism to fuel cancer cell proliferation and drive tumor growth.

Comparative efficacy of four exercise types on obesity-related outcomes in breast cancer survivors: A Bayesian network meta-analysis.

Purpose: Exercise training is associated with improving the prognosis of breast cancer survivors, but no studies have evaluated the optimal exercise intervention. We aimed to investigate the most effective exercise intervention to improve obesity-related outcomes in breast cancer survivors.

Methods: A comprehensive search strategy was conducted in Medline, Embase, Web of Science, Cochrane Library, and Chinese biomedical literature databases from the time of library construction to April 2, 2023.

Creatine kinase B suppresses ferroptosis by phosphorylating GPX4 through a moonlighting function.

Activation of receptor protein kinases is prevalent in various cancers with unknown impact on ferroptosis. Here we demonstrated that AKT activated by insulin-like growth factor 1 receptor signalling phosphorylates creatine kinase B (CKB) T133, reduces metabolic activity of CKB and increases CKB binding to glutathione peroxidase 4 (GPX4). Importantly, CKB acts as a protein kinase and phosphorylates GPX4 S104.

Bioinformatics analysis identified RGS4 as a potential tumor promoter in glioma.

Gliomas is the most common type of intracranial primary malignant tumor and it accounts for ∼80% of primary malignant tumors of the central nervous system. At present, surgical resection with adjuvant radiotherapy and temozolomide adjuvant chemotherapy combined with radiotherapy are the only standard treatments for glioma. However, but overall survival of patients is only 15 months.

Association between sedentary behavior, physical activity, and cardiovascular disease-related outcomes in adults-A meta-analysis and systematic review.

Background: Sedentary behavior (SB) and physical activity (PA) are modifiable risk factors for cardiovascular disease (CVD); however, previous research on the effects of PA and SB on CVD has been relatively homogeneous. Our study investigated the association between PA, SB, and CVD-related outcomes.

Methods: A comprehensive search strategy was conducted in the MEDLINE, Embase, Cochrane Library, and Web of Science databases from their inception to September 2022.

CNNArginineMe: A CNN structure for training models for predicting arginine methylation sites based on the One-Hot encoding of peptide sequence.

Protein arginine methylation (PRme), as one post-translational modification, plays a critical role in numerous cellular processes and regulates critical cellular functions. Though several models for predicting PRme sites have been reported, new models may be required to develop due to the significant increase of identified PRme sites. In this study, we constructed multiple machine-learning and deep-learning models.

Breviscapine remodels myocardial glucose and lipid metabolism by regulating serotonin to alleviate doxorubicin-induced cardiotoxicity.

The broad-spectrum anticancer drug doxorubicin (Dox) is associated with a high incidence of cardiotoxicity, which severely affects the clinical application of the drug and patients' quality of life. Here, we assess how Dox modulates myocardial energy and contractile function and this could aid the development of relevant protective drugs. Mice were subjected to doxorubicin and breviscapine treatment.

Targeting NAD+: is it a common strategy to delay heart aging?

Heart aging is the main susceptible factor to coronary heart disease and significantly increases the risk of heart failure, especially when the aging heart is suffering from ischemia-reperfusion injury. Numerous studies with NAD+ supplementations have suggested its use in anti-aging treatment. However, systematic reviews regarding the overall role of NAD+ in cardiac aging are scarce.

Nanotechnologies for Reactive Oxygen Species"Turn-On" Detection.

Reactive oxygen species (ROS) encompasses a collection of complicated chemical entities characterized by individually specific biological reactivities and physicochemical properties. ROS detection is attracting tremendous attention. The reaction-based nanomaterials for ROS "turn-on" sensing represent novel and efficient tools for ROS detection.

Coupling HDAC4 with transcriptional factor MEF2D abrogates SPRY4-mediated suppression of ERK activation and elicits hepatocellular carcinoma drug resistance.

Hepatocellular carcinoma (HCC) lacks effective treatment, and the patients rapidly develop the acquired resistance to sorafenib with less defined mechanisms. Here, we demonstrate that transcriptional factor myocyte enhancer factor 2D (MEF2D) overexpression is detected in sorafenib-resistant HCC specimens and HCC cell lines and predicts poor prognosis of sorafenib-treated HCC patients. Mechanistically, MEF2D in complex with histone deacetylase HDAC4 directly binds to the SPRY4 promoter regions and suppresses the transcriptional expression of SPRY4, which is a negative regulator of MAPK/ERK signaling pathway.

Fructose and fructose kinase in cancer and other pathologies.

Fructose metabolism and fructose kinase KHK-C/A are key factors in the development of lipid oversynthesis-promoted metabolic disorders and cancer. Here, we summarize and discuss the current knowledge about the specific features of fructose metabolism and the distinct roles of KHK-C and KHK-A in metabolic liver diseases and their relevant metabolic disorders and cancer, and we highlight the specific protein kinase activity of KHK-A in tumor development. In addition, different approaches that have been used to inhibit KHK and the exploration of KHK inhibitors in clinical treatment are introduced.

WNT/β-catenin-suppressed FTO expression increases mA of c-Myc mRNA to promote tumor cell glycolysis and tumorigenesis.

FTO removes the N6-methyladenosine (mA) modification from genes and plays a critical role in cancer development. However, the mechanisms underlying the regulation of FTO and its subsequent impact on the regulation of the epitranscriptome remain to be further elucidated. Here, we demonstrate that FTO expression is downregulated and inversely correlated with poor survival of lung adenocarcinoma patients.

Lipid metabolism and cancer.

Dysregulation in lipid metabolism is among the most prominent metabolic alterations in cancer. Cancer cells harness lipid metabolism to obtain energy, components for biological membranes, and signaling molecules needed for proliferation, survival, invasion, metastasis, and response to the tumor microenvironment impact and cancer therapy. Here, we summarize and discuss current knowledge about the advances made in understanding the regulation of lipid metabolism in cancer cells and introduce different approaches that have been clinically used to disrupt lipid metabolism in cancer therapy.

The Evolving Landscape of Noncanonical Functions of Metabolic Enzymes in Cancer and Other Pathologies.

Key pathological, including oncogenic, signaling pathways regulate the canonical functions of metabolic enzymes that serve the cellular metabolic needs. Importantly, these signaling pathways also confer a large number of metabolic enzymes to have noncanonical or nonmetabolic functions that are referred to as "moonlighting" functions. In this review, we highlight how aberrantly regulated metabolic enzymes with such activities play critical roles in the governing of a wide spectrum of instrumental cellular activities, including gene expression, cell-cycle progression, DNA repair, cell proliferation, survival, apoptosis, and tumor microenvironment remodeling, thereby promoting the pathologic progression of disease, including cancer.

Monoacylglycerol Lipase Knockdown Inhibits Cell Proliferation and Metastasis in Lung Adenocarcinoma.

Abnormal metabolism is one of the hallmarks of cancer cells. Monoacylglycerol lipase (MGLL), a key enzyme in lipid metabolism, has emerged as an important regulator of tumor progression. In this study, we aimed to characterize the role of MGLL in the development of lung adenocarcinoma (LUAD).

A newly discovered role of metabolic enzyme PCK1 as a protein kinase to promote cancer lipogenesis.

Highly active lipogenesis is essential for rapid tumor growth. Sterol regulatory element-binding protein (SREBP) is a key transcriptional factor for lipogenesis and activated by reduced sterol and oxysterol levels. However, the mechanism by which cancer cells activate SREBP without altering these sterol/oxysterol levels remains elusive.

The gluconeogenic enzyme PCK1 phosphorylates INSIG1/2 for lipogenesis.

Cancer cells increase lipogenesis for their proliferation and the activation of sterol regulatory element-binding proteins (SREBPs) has a central role in this process. SREBPs are inhibited by a complex composed of INSIG proteins, SREBP cleavage-activating protein (SCAP) and sterols in the endoplasmic reticulum. Regulation of the interaction between INSIG proteins and SCAP by sterol levels is critical for the dissociation of the SCAP-SREBP complex from the endoplasmic reticulum and the activation of SREBPs.