Mitochondrial Biomarkers and Metabolic Syndrome in Bipolar Disorder DOI Creative Commons

Kassandra A. Zachos,

Jaehyoung Choi, O. Godin

et al.

Psychiatry Research, Journal Year: 2024, Volume and Issue: 339, P. 116063 - 116063

Published: July 6, 2024

The object of this study is test whether mitochondrial blood-based biomarkers are associated with markers metabolic syndrome in bipolar disorder, hypothesizing higher lactate but unchanged cell-free circulating DNA levels disorder patients syndrome. In a cohort study, primary testing from the FondaMental Advanced Centers Expertise for (FACE-BD) was conducted, including 837 stable patients. I-GIVE validation consists 237 participants: and acute patients, non-psychiatric controls, schizophrenia Multivariable regression analyses show significant association triglycerides, fasting glucose systolic diastolic blood pressure. Significantly were presence after adjusting potential confounding factors. Mitochondrial-targeted metabolomics identified distinct metabolite profiles syndrome, differing those without changes Circulating not This thorough analysis indicate associations while showing metabolites can further stratify BD. relevant to improve identification stratification provide personalized-therapeutic opportunities.

Language: Английский

Mitochondrial Dysfunction and Mitophagy in Type 2 Diabetes: Pathophysiology and Therapeutic Targets DOI
Nadezda Apostolova, Teresa Vezza, Jordi Muntané

et al.

Antioxidants and Redox Signaling, Journal Year: 2023, Volume and Issue: 39(4-6), P. 278 - 320

Published: Jan. 15, 2023

Significance: Type 2 diabetes mellitus, which is related to oxidative stress and mitochondrial dysfunction, one of the most prevalent diseases in world. In past decade, alterations autophagy have been shown play a fundamental role development control type diabetes. Further, mitophagy has recognized as key player eliminating dysfunctional mitochondria this disease. Recent Advances: Recently, much progress made understanding molecular events associated with stress, Critical Issues: Despite increasing evidence relationship between their pathophysiolology diabetes, effective therapeutic strategies combat disease through targeting mitochondria, autophagy, are yet be implemented. Future Directions: This review provides wide perspective existing literature concerning complicated interplay mitophagy, dysfunction potential targets based on these mechanisms explored. Antioxid. Redox Signal. 39, 278-320.

Language: Английский

Citations

23

Inflammatory signaling in NASH driven by hepatocyte mitochondrial dysfunctions DOI Creative Commons
Melissa Myint, Francesca Oppedisano, Valeria De Giorgi

et al.

Journal of Translational Medicine, Journal Year: 2023, Volume and Issue: 21(1)

Published: Oct. 26, 2023

Abstract Liver steatosis, inflammation, and variable degrees of fibrosis are the pathological manifestations nonalcoholic steatohepatitis (NASH), an aggressive presentation most prevalent chronic liver disease in Western world known as fatty (NAFL). Mitochondrial hepatocyte dysfunction is a primary event that triggers affecting Kupffer hepatic stellate cell behaviour. Here, we consider role impaired mitochondrial function caused by lipotoxicity during oxidative stress hepatocytes. Dysfunction phosphorylation ROS production cause release damage-associated molecular patterns from dying hepatocytes, leading to activation innate immunity trans-differentiation cells, thereby driving NASH.

Language: Английский

Citations

22

Unraveling the role of NLRP3 inflammasome in allergic inflammation: implications for novel therapies DOI Creative Commons
Hui-Fei Lu,

Yi-Chi Zhou,

Tianyong Hu

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: July 26, 2024

Allergic diseases like asthma, allergic rhinitis and dermatitis pose a significant global health burden, driving the search for novel therapies. The NLRP3 inflammasome, key component of innate immune system, is implicated in various inflammatory diseases. Upon exposure to allergens, undergoes two-step activation process (priming assembly) form active inflammasomes. These inflammasomes trigger caspase-1 activation, leading cleavage pro-inflammatory cytokines (IL-1β IL-18) GSDMD. This induces pyroptosis amplifies inflammation. Recent studies humans mice strongly suggest link between IL-1β, IL-18, development However, further research needed fully understand NLRP3's specific mechanisms allergies. review aims summarize latest advances regulation. We will discuss small molecule drugs natural products targeting as potential therapeutic strategies

Language: Английский

Citations

7

Reframing the link between metabolism and NLRP3 inflammasome: therapeutic opportunities DOI Creative Commons
Miguel Á. Ortega,

Diego De León-Oliva,

Cielo García‐Montero

et al.

Frontiers in Immunology, Journal Year: 2023, Volume and Issue: 14

Published: July 20, 2023

Inflammasomes are multiprotein signaling platforms in the cytosol that senses exogenous and endogenous danger signals respond with maturation secretion of IL-1β IL-18 pyroptosis to induce inflammation protect host. The inflammasome best studied is Nucleotide-binding oligomerization domain, leucine-rich repeat-containing family pyrin domain containing 3 (NLRP3) inflammasome. It activated a two-step process: priming activation, leading sensor NLRP3 recruitment both adaptor ASC executioner pro-caspase 1, which by cleavage. Moreover, activation regulated posttranslational modifications, including ubiquitination/deubiquitination, phosphorylation/dephosphorylation, acetylation/deacetylation, SUMOylation nitrosylation, interaction NLPR3 protein binding partners. connection between it metabolism receiving increasing attention this field. In review, we present structure, functions, regulation NLRP3, special emphasis on mitochondrial dysfunction-mtROS production metabolic signals, i.e., metabolites as well enzymes. By understanding specific inhibitors can be rationally designed for treatment prevention various immune- or metabolic-based diseases. Lastly, review current their mechanism action.

Language: Английский

Citations

14

Mitochondrial Dysfunction is a Crucial Immune Checkpoint for Neuroinflammation and Neurodegeneration: mtDAMPs in Focus DOI
Yogesh Mishra, Ashutosh Kumar, Ravinder K. Kaundal

et al.

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

Published: Aug. 8, 2024

Language: Английский

Citations

6

Neutrophil extracellular traps in central nervous system (CNS) diseases DOI Creative Commons

Bo‐Zong Shao,

Jingjing Jiang, Yicheng Zhao

et al.

PeerJ, Journal Year: 2024, Volume and Issue: 12, P. e16465 - e16465

Published: Jan. 4, 2024

Excessive induction of inflammatory and immune responses is widely considered as one vital factors contributing to the pathogenesis progression central nervous system (CNS) diseases. Neutrophils are well-studied members cell family, innate adaptive immunity. Neutrophil-released neutrophil extracellular traps (NETs) play an important role in regulation various kinds diseases, including CNS In this review, current knowledge on biological features NETs will be introduced. addition, several popular diseases cerebral stroke, Alzheimer’s disease, multiple sclerosis, amyotrophic lateral sclerosis (ALS), neurological cancers described discussed through reviewing previous related studies.

Language: Английский

Citations

5

The trigger for pancreatic disease: NLRP3 inflammasome DOI Creative Commons
Tianming Liu, Qiang Wang,

Zhiwei Du

et al.

Cell Death Discovery, Journal Year: 2023, Volume and Issue: 9(1)

Published: July 14, 2023

Abstract NLRP3 inflammasome is a multiprotein complex expressed in variety of cells to stimulate the production inflammatory factors. Activation depends on regulatory mechanism, and its pro-inflammatory function plays an important role pancreatic diseases. In this literature review, we summarize activation mechanism analyze each four typical Through article, provide relatively comprehensive summary researchers field, some targeted therapy routes.

Language: Английский

Citations

13

Perfluorooctane sulfonate (PFOS) causes aging damage in the liver through the mt-DNA-mediated NLRP3 signaling pathway DOI Creative Commons

Cui Xiaopeng,

Tang Jin

Ecotoxicology and Environmental Safety, Journal Year: 2023, Volume and Issue: 262, P. 115121 - 115121

Published: June 27, 2023

Perfluorooctane sulfonate (PFOS) is not readily degradable in the natural environment, and PFOS widely used industry. Globally, exposure occurs environment. persistent non-biodegradable. The general public can come into contact with by inhaling PFOS-contaminated dust air, drinking contaminated water, eating food. Thus, induces potential health damage globally. In this study, effect of on aging liver was investigated. an vitro cellular model, a series biochemical experiments were conducted via cell proliferation assays, flow cytometry, immunocytochemistry laser confocal microscopy. It found that led to hepatocyte senescence Sa-β-gal staining detection markers (p16, p21 p53). addition, also oxidative stress inflammation. Mechanistic studies have shown lead elevated mitochondrial ROS hepatocytes through calcium overload. cause alterations membrane potential, subsequently inducing mPTP (mitochondrial permeability transition pore) opening, which turn releases mt-DNA from mitochondria cytoplasm, thus activating NLRP3, causes hepatocytes. Based this, we further analyzed vivo caused tissues. On basis, preliminarily investigated β-carotene it could alleviate PFOS. summary, current study shows liver, provides more in-depth understanding toxicity characteristics

Language: Английский

Citations

12

Research Progress of Caspase in Endometriosis DOI
Yuan Yang, Leilei Li,

Yu-Xin Qi

et al.

Reproductive Sciences, Journal Year: 2024, Volume and Issue: 31(6), P. 1496 - 1507

Published: Feb. 12, 2024

Language: Английский

Citations

4

Effects of the Glucocorticoid-Mediated Mitochondrial Translocation of Glucocorticoid Receptors on Oxidative Stress and Pyroptosis in BV-2 Microglia DOI
Ruonan Dang,

Xuyang Hou,

Xinglan Huang

et al.

Journal of Molecular Neuroscience, Journal Year: 2024, Volume and Issue: 74(1)

Published: March 13, 2024

Language: Английский

Citations

4