Frontiers in Endocrinology, Год журнала: 2024, Номер 15
Опубликована: Дек. 9, 2024
Diabetes has emerged as the foremost public health challenge of 21st century, with a notable shift towards managing it through an inflammatory lens. This study seeks to investigate role NLRP3 infalmmasome in diabetes over past ten years, leveraging bibliometric analysis pinpoint prevailing trends, underscore critical focal points, and establish roadmap for subsequent research endeavors.
Язык: Английский
European Journal of Heart Failure, Год журнала: 2025, Номер unknown
Опубликована: Янв. 14, 2025
Aims Hyperglycaemic conditions increase cardiac stress, a common phenomenon associated with inflammation, aging, and metabolic imbalance. Sodium–glucose cotransporter 2 inhibitors, class of anti‐diabetic drugs, showed to improve cardiovascular functions although their mechanism action has not yet been fully established. This study investigated the effects empagliflozin on cardiomyocytes following high glucose exposure, specifically focusing inflammatory responses. Methods results A three‐part strategy was formulated: (i) meta‐analysis selected randomized clinical trials carried out assess anti‐inflammatory in diabetic patients; (ii) impact human cardiomyocyte AC16 cells exposed normal (5 mM) (33 concentrations for 7 days explored by evaluating gene expression protein levels pivotal markers endoplasmic reticulum damage, calcium modulation; (iii) silico data from bioinformatic analyses were exploited construct an interaction map delineating potential tissue. Empagliflozin reversed high‐glucose mediated alterations at transcriptional level, decreasing inflammatory, metabolic, aging signatures. Specifically, vitro experiments cardiomyocytes, meta‐analyses biomarkers peripheral blood samples, sequencing pathological heart tissues, all support that exerts both systemically directly tissue, cardiomyocytes. Conclusion Our provides insights based robust mechanistic optimizing failure management highlights intricate interplay between diabetes, health.
Язык: Английский
Процитировано
2
Diagnostics, Год журнала: 2024, Номер 14(21), С. 2453 - 2453
Опубликована: Ноя. 1, 2024
Type 2 diabetes mellitus is a complex metabolic disorder characterized by insulin resistance and, subsequently, decreased secretion. This condition closely linked to obesity, major risk factor that boosts the development of chronic systemic inflammation, which, in turn, recognized for its crucial role onset resistance. Under conditions adipose tissue, particularly visceral fat, becomes an active endocrine organ releases wide range pro-inflammatory mediators, including cytokines, chemokines, and adipokines. These along with cluster differentiation (CD) markers, contribute maintenance low-grade promote cellular signaling facilitate infiltration inflammatory cells into tissues. Emerging studies have indicated accumulation new cell population tissue these conditions, known as myeloid-derived suppressor (MDSCs). possess ability suppress immune system, impacting obesity-related inflammation. Given limited literature addressing MDSCs context type diabetes, this article aims explore interaction between MDSC activity. Identifying understanding immature essential not only improving management but also potential targeted therapeutic strategies aimed at both glycemic control reduction associated
Язык: Английский
Процитировано
5
Frontiers in Microbiology, Год журнала: 2025, Номер 16
Опубликована: Янв. 29, 2025
The gut microbiota plays a pivotal role in human metabolic health by influencing immune responses, digestion, and homeostasis. Recent research highlights the intricate interactions between RNA, especially non-coding RNAs, regulating processes. Dysbiosis of has been linked to disorders such as type 2 diabetes, obesity, metabolic-associated fatty liver disease (MAFLD) heart disease. Microbial metabolites, including short-chain acids (SCFAs), modulate RNA expression, lipid metabolism, glucose regulation, inflammatory responses. Additionally, microRNAs (miRNAs) long RNAs (lncRNAs) serve critical regulators these processes, with emerging evidence showing that gut-derived metabolites affect post-transcriptional gene regulation. This review synthesizes current understanding microbiota-RNA axis its diseases. By exploring molecular mechanisms, particularly how microbiota-derived signals pathways, underscores potential targeting this for therapeutic interventions. Furthermore, it examines dysbiosis leads epigenetic changes m6A methylation, contributing pathogenesis. These insights offer new perspective on prevention treatment diseases, applications personalized medicine.
Язык: Английский
Процитировано
0
Frontiers in Endocrinology, Год журнала: 2025, Номер 16
Опубликована: Фев. 25, 2025
As a multidimensional metabolic disorder, the disability and death rate of type 2 diabetes mellitus (T2DM) has increased over time. T2DM covers wide range pathological manifestations ranging from hyperglycemia to multi-organ failure, it potential evolve into acute complications, including ketosis chronic complications such as peripheral neuropathy, retinopathy, nephropathy. mainly occurs in microvascular large vessels thus is restricted for clinician diagnose prescribe. However, mechanism clinical diagnosis are inadequate. High-throughput metabolomics, characterized by non-invasive diagnostic techniques identify biomarkers distinct stages T2DM, been increasingly recognized vigorous tool with latent capacity translation. The stratification can significantly reduce mortality rates. By tracing metabolome associated pathways impaired fasting blood glucose or tolerance severe organ chief contributions large, independent population-based cohorts summarized herein. These results facilitate understanding pathophysiology supports research accurate diagnosis, risk prediction, curative effect, stages, prognosis judgment T2DM.
Язык: Английский
Процитировано
0
Cardiovascular Diabetology, Год журнала: 2025, Номер 24(1)
Опубликована: Май 14, 2025
Abstract Background Type 2 diabetes mellitus (T2DM) represents a significant risk factor for cardiovascular disease, particularly heart failure with preserved ejection fraction (HFpEF). HFpEF predominantly affects elderly individuals and women, is characterized by dysfunctions associated metabolic, inflammatory, oxidative stress pathways. Despite being the most prevalent phenotype in patients T2DM, its underlying pathophysiological mechanisms remain inadequately elucidated. Objective This study aims to investigate effects of on myocardial inflammation, stress, protein quality control (PQC) HFpEF, particular emphasis insulin signaling, autophagy, chaperone-mediated responses. Methods We conducted an analysis left ventricular tissue from patients, both without diabetes, employing range molecular, biochemical, functional assays. The passive stiffness cardiomyocytes (Fpassive) was assessed demembranated before after implementing treatments aimed at reducing inflammation (IL-6 inhibition), (Mito-TEMPO), enhancing PQC (HSP27, HSP70). Inflammatory markers (NF-κB, IL-6, TNF-α, ICAM-1, VCAM-1, NLRP3), (ROS, GSH/GSSG ratio, lipid peroxidation), components signaling pathways (PI3K/AKT/mTOR, AMPK, MAPK, PKG) were evaluated using western blotting, immunofluorescence, ELISA techniques. Results Hearts diabetic exhibited significantly heightened upregulation NF-κB, NLRP3 inflammasome. increase accompanied elevated diminished nitric oxide (NO) bioavailability, impaired activation NO-sGC-cGMP-PKG pathway. Notably, dysregulation observed, as indicated decreased AKT phosphorylation autophagy regulation mediated AMPK mTOR. Additionally, dysfunction evidenced reduced expression levels HSP27 HSP70, which correlated increased cardiomyocyte stiffness. Targeted therapeutic interventions effectively Fpassive, IL-6 inhibition, Mito-TEMPO, HSP administration leading improvements mechanical properties. Conclusion findings this elucidate mechanistic relationship among impairment context HFpEF. Therapeutic strategies that target these dysregulated pathways, including mitochondrial antioxidants, protection, may enhance function T2DM. Addressing molecular could facilitate development novel specifically tailored population. Graphical abstract
Язык: Английский
Процитировано
0
Clinical and Experimental Hypertension, Год журнала: 2024, Номер 47(1)
Опубликована: Дек. 26, 2024
This study investigated the impact of maternal high-fat diet on vascular function and endothelial homeostasis in offspring. We found that offspring exposed to exhibited elevated blood pressure, impaired abdominal aortic function, imbalance. These changes were accompanied by increased levels reactive oxygen species (ROS) upregulation pro-inflammatory cytokines (including IL-1β, TNF-α, IL-6, IL-10). Treatment with NLRP3 or IL-1β inhibitors prevented deterioration reduced NO production, inflammation induced exposure compared control group. The findings suggest during pregnancy, mitigating impairments can be achieved inhibiting NLRP3/IL-1β pathway.
Язык: Английский
Процитировано
2
Frontiers in Endocrinology, Год журнала: 2024, Номер 15
Опубликована: Дек. 9, 2024
Diabetes has emerged as the foremost public health challenge of 21st century, with a notable shift towards managing it through an inflammatory lens. This study seeks to investigate role NLRP3 infalmmasome in diabetes over past ten years, leveraging bibliometric analysis pinpoint prevailing trends, underscore critical focal points, and establish roadmap for subsequent research endeavors.
Язык: Английский
Процитировано
0