Unraveling the cGAS/STING signaling mechanism: impact on glycerolipid metabolism and diseases DOI Creative Commons
Jie Su,

Fuyu Cheng,

Wei Yuan

et al.

Frontiers in Medicine, Journal Year: 2024, Volume and Issue: 11

Published: Nov. 28, 2024

The cyclic GMP-AMP synthase (cGAS) and its downstream effector, the stimulator of interferon genes (STING), are crucial components innate immune response, traditionally recognized for their role in detecting cytosolic DNA from pathogens damaged host cells. However, recent research indicates that cGAS-STING pathway also significantly impacts metabolic processes, particularly glycerolipid metabolism. Glycerolipids essential energy storage cellular membrane integrity, dysregulation is linked to disorders such as obesity, insulin resistance, non-alcoholic fatty liver disease (NAFLD). Both cGAS STING expressed various tissues, suggesting a potential lipid homeostasis. Chronic activation may promote inflammatory states exacerbate resistance accumulation, forming feedback loop dysfunction. This review explores emerging relationship between cGAS/STING signaling metabolism, discussing mechanisms through which this influences regulation therapeutic interventions. By integrating insights immunology we aim provide comprehensive understanding how axis serve novel target addressing enhancing health outcomes.

Language: Английский

Macrophage plasticity: signaling pathways, tissue repair, and regeneration DOI Creative Commons
Lingfeng Yan,

Jue Wang,

Xin Cai

et al.

MedComm, Journal Year: 2024, Volume and Issue: 5(8)

Published: Aug. 1, 2024

Abstract Macrophages are versatile immune cells with remarkable plasticity, enabling them to adapt diverse tissue microenvironments and perform various functions. Traditionally categorized into classically activated (M1) alternatively (M2) phenotypes, recent advances have revealed a spectrum of macrophage activation states that extend beyond this dichotomy. The complex interplay signaling pathways, transcriptional regulators, epigenetic modifications orchestrates polarization, allowing respond stimuli dynamically. Here, we provide comprehensive overview the cascades governing focusing on roles Toll‐like receptors, signal transducer activator transcription proteins, nuclear microRNAs. We also discuss emerging concepts metabolic reprogramming trained immunity, contributing their functional adaptability. Macrophage plasticity plays pivotal role in repair regeneration, macrophages coordinating inflammation, angiogenesis, matrix remodeling restore homeostasis. By harnessing potential novel therapeutic strategies targeting polarization could be developed for diseases, including chronic wounds, fibrotic disorders, inflammatory conditions. Ultimately, deeper understanding molecular mechanisms underpinning will pave way innovative regenerative medicine engineering approaches.

Language: Английский

Citations

27
IL-17 in wound repair: bridging acute and chronic responses DOI Creative Commons
Xingrui Mu,

Rifang Gu,

Ming Tang

et al.

Cell Communication and Signaling, Journal Year: 2024, Volume and Issue: 22(1)

Published: May 27, 2024

Abstract Chronic wounds, resulting from persistent inflammation, can trigger a cascade of detrimental effects including exacerbating inflammatory cytokines, compromised blood circulation at the wound site, elevation white cell count, increased reactive oxygen species, and potential risk bacterial infection. The interleukin-17 (IL-17) signaling pathway, which plays crucial role in regulating immune responses, has been identified as promising target for treating skin diseases. This review aims to delve deeper into pathological molecular mechanisms IL-17 family its pathways repair. intricate interactions between other cytokines will be discussed detail, along with activation various pathways, provide comprehensive understanding IL-17’s involvement chronic inflammation

Language: Английский

Citations

8
Regulatory T cell-based therapy in type 1 diabetes: Latest breakthroughs and evidence DOI

Qiongxiao Huang,

Jing Zhu

International Immunopharmacology, Journal Year: 2024, Volume and Issue: 140, P. 112724 - 112724

Published: Aug. 3, 2024

Language: Английский

Citations

6
Cardiomyocyte-specific deletion of STING improves cardiac function, glucose homeostasis, and wound healing in diabetic mice DOI
Xiaorong Li, Kai Guo,

Qingju Zhou

et al.

Life Sciences, Journal Year: 2025, Volume and Issue: unknown, P. 123470 - 123470

Published: Feb. 1, 2025

Language: Английский

Citations

0
Novel impact of metal ion-induced cell death on diabetic cardiomyopathy pathogenesis and therapy DOI

Jingjing Jiang,

Shengnan Hu, Kaibo Hu

et al.

APOPTOSIS, Journal Year: 2025, Volume and Issue: unknown

Published: March 5, 2025

Language: Английский

Citations

0
Nano-Delivery of STING Agonists: Unraveling the Potential of Immunotherapy DOI
Meng Zhang,

Yating Ji,

Mingxia Liu

et al.

Acta Biomaterialia, Journal Year: 2025, Volume and Issue: unknown

Published: March 1, 2025

Language: Английский

Citations

0
Revolutionizing Diabetic Foot Ulcer Care: The Senotherapeutic Approach DOI Creative Commons
Guiqin Zhang,

Priyadarshani Nadeeshika Samarawickrama,

Li Gui

et al.

Aging and Disease, Journal Year: 2024, Volume and Issue: unknown, P. 0 - 0

Published: Jan. 1, 2024

Diabetic foot ulcers (DFUs) are a prevalent and profoundly debilitating complication that afflicts individuals with diabetes mellitus (DM). These associated substantial morbidity, recurrence rates, disability, mortality, imposing economic, psychological, medical burdens. Timely detection intervention can mitigate the morbidity disparities linked to DFU. Nevertheless, current therapeutic approaches for DFU continue grapple multifaceted limitations. A growing body of evidence emphasizes crucial role cellular senescence in pathogenesis chronic wounds. Interventions try delay senescence, eliminate senescent cells (SnCs), or suppress senescence-associated secretory phenotype (SASP) have shown promise helping wounds heal. In this context, targeting emerges as novel strategy comprehensive review, we look at pathology treatment systematic way. We also explain importance investigating SnCs highlight great potential senotherapeutics target treatment. The development efficacious safe represents pioneering approach aimed enhancing quality life affected by

Language: Английский

Citations

2
Identification of CXCL13 as a Promising Biomarker for Immune Checkpoint Blockade Therapy and PARP Inhibitor Therapy in Ovarian Cancer DOI
Yue Ding, Ye Zheng, Bo Ding

et al.

Molecular Biotechnology, Journal Year: 2024, Volume and Issue: unknown

Published: June 10, 2024

Language: Английский

Citations

2
The cGAS-STING Pathway: A New Therapeutic Target for Ischemia–Reperfusion Injury in Acute Myocardial Infarction? DOI Creative Commons

Mengxiang Tian,

Fengyuan Li,

Haiping Pei

et al.

Biomedicines, Journal Year: 2024, Volume and Issue: 12(8), P. 1728 - 1728

Published: Aug. 2, 2024

The innate immune system is the body's natural defense system, which recognizes a wide range of microbial molecules (such as bacterial DNA and RNA) abnormal within cells misplaced DNA, self-antigens) to play its role. released into cytoplasm activates cyclic GMP-AMP synthase (cGAS)-stimulator interferon genes (STING) signaling pathway initiate an response. Ischemia-reperfusion injury (IRI) after acute myocardial infarction refers phenomenon where tissue suffers further damage upon restoration blood flow. This issue significant clinical problem in treatment infarction, it can diminish effectiveness reperfusion therapy lead deterioration cardiac function. Studies have found that cGAS-STING closely related this phenomenon. Therefore, review aims describe role ischemia-reperfusion summarize current development status inhibitors application nanomaterials elucidate potential therapeutic target.

Language: Английский

Citations

2
PLAGL1 overexpression induces cytoplasmic DNA accumulation that triggers cGAS/STING activation DOI Creative Commons

Cheng Li,

Lingyan Qiao,

Juan Ge

et al.

Journal of Cellular and Molecular Medicine, Journal Year: 2024, Volume and Issue: 28(19)

Published: Oct. 1, 2024

Abstract Pancreatic β‐cell damage mediated by apoptosis is believed to be a main trigger of type 1 diabetes mellitus (T1DM), which proposed as an organ‐specific autoimmune disease T cells. Nonetheless, the fundamental origins T1DM remain uncertain. Here, we illustrate that increase in PLAGL1 expression induces apoptosis, evidenced mitochondrial membrane impairment and nucleolar degradation. The gene levels from cDNA samples were determined using qRT‐PCR method. Western blot Co‐immunoprecipitation applied for protein interactions, respectively. Flow cytometry TUNEL assay used detect pancreatic β cell apoptosis. Female NOD/LtJ mice with recent‐onset has been vivo studies. Glucose‐stimulated insulin secretion (GSIS) glucose tolerance test (GTT) method islet function assessment. Haematoxylin Eosin (H&E) Immunohistochemistry (IHC) performed evalute histological improvement beta. Subsequent cytoplasmic DNA accumulation triggers senser, cyclic guanosine monophosphate‐AMP synthase (cGAS)‐stimulator interferon genes (STING) pathway. STING activation further stimulates downstream IRF3 NF‐kB pathways, thus boost type‐I signalling inflammation. These findings elucidate molecular mechanism linking induced suggest potential benefit targeting cGAS/STING treatment.

Language: Английский

Citations

1