Diagnostic Accuracy of Computational Fluid Dynamics-Based Fractional Flow Reserve Derived From Coronary Angiography: The ACCURATE Study.

Background: Although fractional flow reserve (FFR) is the contemporary standard to detect hemodynamically significant coronary stenosis, it remains underused for the need of pressure wire and hyperemic stimulus. Coronary angiography-derived FFR could break through these barriers. The aim of this study was to assess the feasibility and performance of a novel diagnostic modality deriving FFR from invasive coronary angiography (AccuFFRangio) for coronary physiological assessment.

Physiological, transcriptomic, and metabolomic analyses of the chilling stress response in two melon (Cucumis melo L.) genotypes.

Background: Chilling stress is a key abiotic stress that severely restricts the growth and quality of melon (Cucumis melo L.). Few studies have investigated the mechanism of response to chilling stress in melon.

Role of intestinal testosterone-degrading bacteria and 3/17β-HSD in the pathogenesis of testosterone deficiency-induced hyperlipidemia in males.

Testosterone deficiency can cause abnormal lipid metabolism in men, leading to hyperlipidemia. We identified the testosterone-degrading bacterium Pseudomonas nitroreducens in the fecal samples of male patients with hyperlipidemia. Gastric administration of P.

LC3B-regulated autophagy mitigates zinc oxide nanoparticle-induced epithelial cell dysfunction and acute lung injury.

Zinc oxide nanoparticles (ZnONPs) are widely utilized across various industries, raising concerns about their potential toxicity, especially in the respiratory system. This study explores the role of autophagy, regulated by microtubule-associated protein 1A/1B-light chain 3B (LC3B), in ZnONPs-induced toxicity using both in vivo (LC3B knockout mice) and in vitro (BEAS-2B cells) models. Our findings demonstrate that LC3B-regulated autophagy mitigates ZnONPs-induced epithelial cell dysfunction and acute lung injury.

Ginkgo Biloba Bioactive Phytochemicals against Age-Related Diseases: Evidence from a Stepwise, High-Throughput Research Platform.

The seeds of ginkgo biloba L (GB) have been widely used worldwide. This study investigated the bioefficacies of whole GB seed powder (WGP) retaining the full nutrients of ginkgo against aging, atherosclerosis, and fatigue. The experimental results indicated that WGP lowered brain monoamine oxidase and serum malondialdehyde levels, enhanced thymus/spleen indexes, and improved learning ability, and delayed aging in senescent mice.

Metabolic landscape in venous thrombosis: insights into molecular biology and therapeutic implications.

The findings of the last decade suggest a complex link between inflammatory cells, coagulation, and the activation of platelets and their synergistic interaction to promote venous thrombosis. Inflammation is present throughout the process of venous thrombosis, and various metabolic pathways of erythrocytes, endothelial cells, and immune cells involved in venous thrombosis, including glucose metabolism, lipid metabolism, homocysteine metabolism, and oxidative stress, are associated with inflammation. While the metabolic microenvironment has been identified as a marker of malignancy, recent studies have revealed that for cancer thrombosis, alterations in the metabolic microenvironment appear to also be a potential risk.

N6-methyladenosine demethylase FTO regulates neuronal oxidative stress via YTHDC1-ATF3 axis in arsenic-induced cognitive dysfunction.

Excessive exposure to metals in daily life has been proposed as an environmental risk factor for neurological disorders. Oxidative stress is an inevitable stage involved in the neurotoxic effects induced by metals, nevertheless, the underlying mechanisms are still unclear. In this study, we used arsenic as a representative environmental heavy metal to induce neuronal oxidative stress and demonstrated that both in vitro and in vivo exposure to arsenic significantly increased the level of N6-methyladenosine (m6A) by down-regulating its demethylase FTO.

[Retracted] MicroRNA-124-3p inhibits the growth and metastasis of nasopharyngeal carcinoma cells by targeting STAT3.

Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the cell apoptotic data in Fig. 4 on p. 1389 and the migration and invasion assay data shown in Figs.

Association between protein-to-energy ratio and overweight/obesity in children and adolescents in the United States: a cross-sectional study based on NHANES.

Background: The dietary protein proportion may be crucial in triggering overweight and obesity among children and adolescents.

Methods: Cross-sectional data from 4,336 children and adolescents who participated in the National Health and Nutrition Survey (NHANES) between 2011 and March 2020 were analyzed. Multivariate logistic regression was used to calculate odds ratio (OR) and 95% confidence interval (CI).

SUMOylation modification of FTO facilitates oxidative damage response of arsenic by IGF2BP3 in an m6A-dependent manner.

N6-methyladenosine (m6A) is the most common form of internal post-transcriptional methylation observed in eukaryotic mRNAs. The abnormally increased level of m6A within the cells can be catalyzed by specific demethylase fat mass and obesity-associated protein (FTO) and stay in a dynamic and reversible state. However, whether and how FTO regulates oxidative damage via m6A modification remain largely unclear.

NBR1-mediated autophagic degradation of caspase 8 protects vascular endothelial cells against arsenite-induced apoptotic cell death.

Vascular endothelial cells play a critical role in maintaining the health of blood vessels, but dysfunction can lead to cardiovascular diseases. The impact of arsenite exposure on cardiovascular health is a significant concern due to its potential adverse effects. This study aims to explore how NBR1-mediated autophagy in vascular endothelial cells can protect against oxidative stress and apoptosis induced by arsenite.

The burden and management competency of cardiomyopathies in China: a nationwide survey study.

Background: The public health burden of cardiomyopathies and competency in their management by health agencies in China are not well understood.

Methods: This study adopted a multi-stage sampling method for hospital selection. In the first stage, nationwide tertiary hospital recruitment was performed.

Blockade of endothelial adenosine receptor 2 A suppresses atherosclerosis in vivo through inhibiting CREB-ALK5-mediated endothelial to mesenchymal transition.

Cardiovascular diseases (CVDs) are the leading cause of death worldwide, and morbidity and mortality rates continue to rise. Atherosclerosis constitutes the principal etiology of CVDs. Endothelial injury, inflammation, and dysfunction are the initiating factors of atherosclerosis.

GAS41 modulates ferroptosis by anchoring NRF2 on chromatin.

YEATS domain-containing protein GAS41 is a histone reader and oncogene. Here, through genome-wide CRISPR-Cas9 screenings, we identify GAS41 as a repressor of ferroptosis. GAS41 interacts with NRF2 and is critical for NRF2 to activate its targets such as SLC7A11 for modulating ferroptosis.

Ferroptosis: Biology and Role in Gastrointestinal Disease.

Ferroptosis is a form of nonapoptotic cell death that involves iron-dependent phospholipid peroxidation induced by accumulation of reactive oxygen species, and results in plasma membrane damage and the release of damage-associated molecular patterns. Ferroptosis has been implicated in aging and immunity, as well as disease states including intestinal and liver conditions and cancer. To date, several ferroptosis-associated genes and pathways have been implicated in liver disease.

A guideline on the molecular ecosystem regulating ferroptosis.

Ferroptosis, an intricately regulated form of cell death characterized by uncontrolled lipid peroxidation, has garnered substantial interest since this term was first coined in 2012. Recent years have witnessed remarkable progress in elucidating the detailed molecular mechanisms that govern ferroptosis induction and defence, with particular emphasis on the roles of heterogeneity and plasticity. In this Review, we discuss the molecular ecosystem of ferroptosis, with implications that may inform and enable safe and effective therapeutic strategies across a broad spectrum of diseases.

Phospholipids with two polyunsaturated fatty acyl tails promote ferroptosis.

Phospholipids containing a single polyunsaturated fatty acyl tail (PL-PUFAs) are considered the driving force behind ferroptosis, whereas phospholipids with diacyl-PUFA tails (PL-PUFAs) have been rarely characterized. Dietary lipids modulate ferroptosis, but the mechanisms governing lipid metabolism and ferroptosis sensitivity are not well understood. Our research revealed a significant accumulation of diacyl-PUFA phosphatidylcholines (PC-PUFAs) following fatty acid or phospholipid treatments, correlating with cancer cell sensitivity to ferroptosis.

When CDK4/6i meets GPX4i: Stop dividing to die iron hard.

In this issue of Cell Chemical Biology, Rodencal et al. report that cell-cycle arrest by p53 stabilizers or CDK4/6 inhibitors (CDK4/6i) can lead to phospholipid remodeling and hence sensitize cancer cells to GPX4 inhibitor (GPX4i)-triggered ferroptosis. This study suggests a novel cancer therapeutic strategy combining CDK4/6i with GPX4i.

PHLDA2-mediated phosphatidic acid peroxidation triggers a distinct ferroptotic response during tumor suppression.

Although the role of ferroptosis in killing tumor cells is well established, recent studies indicate that ferroptosis inducers also sabotage anti-tumor immunity by killing neutrophils and thus unexpectedly stimulate tumor growth, raising a serious issue about whether ferroptosis effectively suppresses tumor development in vivo. Through genome-wide CRISPR-Cas9 screenings, we discover a pleckstrin homology-like domain family A member 2 (PHLDA2)-mediated ferroptosis pathway that is neither ACSL4-dependent nor requires common ferroptosis inducers. PHLDA2-mediated ferroptosis acts through the peroxidation of phosphatidic acid (PA) upon high levels of reactive oxygen species (ROS).