APOPTOSIS, Journal Year: 2023, Volume and Issue: 29(1-2), P. 3 - 21
Published: Oct. 17, 2023
Language: Английский
APOPTOSIS, Journal Year: 2023, Volume and Issue: 29(1-2), P. 3 - 21
Published: Oct. 17, 2023
Language: Английский
International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(9), P. 7910 - 7910
Published: April 26, 2023
Recent advances have greatly improved our understanding of the molecular mechanisms behind atherosclerosis pathogenesis. However, there is still a need to systematize this data from general pathology perspective, particularly with regard atherogenesis patterns in context both canonical and non-classical inflammation types. In review, we analyze various typical phenomena outcomes cellular pro-inflammatory stress atherosclerosis, as well role endothelial dysfunction local systemic manifestations low-grade inflammation. We also present features immune development productive stable unstable plaques, along their similarities differences compared There are numerous factors that act inducers inflammatory process including vascular endothelium aging, metabolic dysfunctions, autoimmune, some cases, infectious damage factors. Life-critical complications such cardiogenic shock severe strokes, associated acute hyperinflammation. Additionally, critical atherosclerotic ischemia lower extremities induces paracoagulation chronic Conversely, sepsis, other conditions, diseases contribute atherogenesis. summary, can be characterized an independent form inflammation, sharing but having fundamental variants (classic vasculitis).
Language: Английский
Citations
119Cell Death and Disease, Journal Year: 2023, Volume and Issue: 14(10)
Published: Oct. 20, 2023
Abstract Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of fatty deposits in inner walls vessels. These plaques restrict blood flow and lead to complications such as heart attack or stroke. The development atherosclerosis influenced variety factors, including age, genetics, lifestyle, underlying health conditions high pressure diabetes. Atherosclerotic stable form are slow growth, which leads luminal stenosis, with low embolic potential unstable form, contributes risk for thrombotic rapid clinical onset. In this complex scenario atherosclerosis, macrophages participate whole process, initiation, growth eventually rupture wound healing stages artery plaque formation. Macrophages exhibit heterogeneity plasticity, affect evolving microenvironment, e.g., leading excessive lipid accumulation, cytokine hyperactivation, hypoxia, apoptosis necroptosis. metabolic functional transitions response microenvironmental factors not only influence ongoing imminent responses within lesions but also directly dictate atherosclerotic progression regression. review, we discuss origin plaques, their phenotypic diversity, shifts, fate roles they play dynamic atherosclerosis. It describes how interact other cells, particularly T cells. Ultimately, targeting pathways involved macrophage polarization may innovative promising approaches precision medicine. Further insights into landscape biological features offer valuable information optimizing future treatment macrophages.
Language: Английский
Citations
116Cancer Gene Therapy, Journal Year: 2024, Volume and Issue: 31(7), P. 970 - 983
Published: March 29, 2024
Abstract This comprehensive review explores the intricate mechanisms of PANoptosis and its implications in cancer. PANoptosis, a convergence apoptosis, pyroptosis, necroptosis, plays crucial role cell death immune response regulation. The study delves into molecular pathways each mechanism their crosstalk within emphasizing shared components like caspases PANoptosome complex. It highlights significant various cancers, including respiratory, digestive, genitourinary, gliomas, breast showing impact on tumorigenesis patient survival rates. We further discuss interwoven relationship between tumor microenvironment (TME), illustrating how influences behavior progression. underscores dynamic interplay tumors microenvironments, focusing roles different cells interactions with cancer cells. Moreover, presents new breakthroughs therapy, potential targeting to enhance anti-tumor immunity. outlines strategies manipulate for therapeutic purposes, such as key signaling molecules caspases, NLRP3, RIPK1, RIPK3. novel treatments immunogenic PANoptosis-initiated therapies nanoparticle-based is also explored.
Language: Английский
Citations
35Journal of Atherosclerosis and Thrombosis, Journal Year: 2024, Volume and Issue: 31(3), P. 189 - 200
Published: Jan. 13, 2024
The detrimental effects of cigarette smoking on cardiovascular health, particularly atherosclerosis and thrombosis, are well established, more detailed mechanisms continue to emerge. As the fundamental pathophysiology adverse smoking, endothelial dysfunction, inflammation, thrombosis considered be important. Cigarette smoke induces leading impaired vascular dilation hemostasis regulation. Factors contributing dysfunction include reduced bioavailability nitric oxide, increased levels superoxide anion, endothelin release. Chronic inflammation wall is a central pathogenesis smoking-induced atherosclerosis. Smoking systemically elevates inflammatory markers expression adhesion molecules cytokines in various tissues. Pattern recognition receptors damage-associated molecular patterns play crucial roles mechanism underlying inflammation. Smoking-induced DNA damage activation innate immunity, such as NLRP3 inflammasome, cyclic GMP-AMP synthase (cGAS)-stimulator interferon genes (STING) pathway, Toll-like receptor 9, shown amplify cytokine expression. smoke-induced oxidative stress influence platelet adhesion, aggregation, coagulation via molecule upregulation. Furthermore, it affects cascade fibrinolysis balance, causing thrombus formation. Matrix metalloproteinases contribute plaque vulnerability atherothrombotic events. impact cells further intensifies risk atherothrombosis. Collectively, exposure exerts profound function, development progression diseases. Understanding these intricate highlights urgent need for cessation protect health. This comprehensive review investigates multifaceted through which contributes life-threatening conditions.
Language: Английский
Citations
33Military Medical Research, Journal Year: 2024, Volume and Issue: 11(1)
Published: May 29, 2024
Abstract Mitochondria, the most crucial energy-generating organelles in eukaryotic cells, play a pivotal role regulating energy metabolism. However, their significance extends beyond this, as they are also indispensable vital life processes such cell proliferation, differentiation, immune responses, and redox balance. In response to various physiological signals or external stimuli, sophisticated mitochondrial quality control (MQC) mechanism has evolved, encompassing key like biogenesis, dynamics, mitophagy, which have garnered increasing attention from researchers unveil specific molecular mechanisms. this review, we present comprehensive summary of primary mechanisms functions regulators involved major components MQC. Furthermore, critical regulated by MQC its diverse roles progression systemic diseases been described detail. We discuss agonists antagonists targeting MQC, aiming explore potential therapeutic research prospects enhancing stabilize function.
Language: Английский
Citations
32Cell Death Discovery, Journal Year: 2024, Volume and Issue: 10(1)
Published: Jan. 13, 2024
Abstract Copper is an essential micronutrient that plays a pivotal role in numerous physiological processes virtually all cell types. Nevertheless, the dysregulation of copper homeostasis, whether towards excess or deficiency, can lead to pathological alterations, such as atherosclerosis. With advent concept copper-induced death, termed cuproptosis, researchers have increasingly focused on potential dyshomeostasis In this review, we provide broad overview cellular and systemic metabolism. We then summarize evidence linking atherosclerosis elucidate mechanisms underlying development terms both deficiency. Furthermore, discuss for its interactions with other modes highlight cuproptosis-related mitochondrial dysfunction Finally, explore therapeutic strategy targeting novel form aiming some insights management
Language: Английский
Citations
28Journal of Advanced Research, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 1, 2025
The modification of endothelial cells (ECs) biological function under pathogenic conditions leads to the expression mesenchymal stromal (MSCs) markers, defined as endothelial-to-mesenchymal transition (EndMT). Invisible in onset and slow progression, atherosclerosis (AS) is a potential contributor various atherosclerotic cardiovascular diseases (ASCVD). By triggering AS, EndMT, "initiator" induces progression ASCVD such coronary heart disease (CHD) ischemic cerebrovascular (ICD), with serious clinical complications myocardial infarction (MI) stroke. In-depth research pathomechanisms EndMT identification targeted therapeutic strategies hold considerable value for prevention treatment ASCVD-associated delayed EndMT. Although previous studies have progressively unraveled complexity its pathogenicity triggered by alterations vascular microenvironmental factors, systematic descriptions most recent roles strategies, their future directions are scarce.
Language: Английский
Citations
2Frontiers in Immunology, Journal Year: 2025, Volume and Issue: 15
Published: Jan. 17, 2025
High-grade serous ovarian cancer (HGSOC), the predominant subtype of epithelial cancer, is frequently diagnosed at an advanced stage due to its nonspecific early symptoms. Despite standard treatments, including cytoreductive surgery and platinum-based chemotherapy, significant improvements in survival have been limited. Understanding molecular mechanisms, immune landscape, drug sensitivity HGSOC crucial for developing more effective personalized therapies. This study integrates insights from immunology, profiling, analysis identify novel therapeutic targets improve treatment outcomes. Utilizing single-cell RNA sequencing (scRNA-seq), systematically examines tumor heterogeneity microenvironment, focusing on biomarkers influencing response activity, aiming enhance patient outcomes quality life. scRNA-seq data was obtained GEO database this study. Differential gene expression analyzed using ontology set enrichment methods. InferCNV identified malignant cells, while Monocle, Cytotrace, Slingshot software inferred differentiation trajectories. The CellChat package predicted cellular communication between cell subtypes other pySCENIC utilized transcription factor regulatory networks within subtypes. Finally, results were validated through functional experiments, a prognostic model developed assess prognosis, infiltration, across various risk groups. investigated scRNA-seq, their interactions microenvironment. We confirmed key role C2 IGF2+ HGSOC, which significantly associated with poor prognosis high levels chromosomal copy number variations. located terminal tumor, displaying higher degree malignancy close association IIIC tissue types. also metabolic pathways, such as glycolysis riboflavin metabolism, well programmed death processes. highlighted complex fibroblasts MK signaling pathway, may be closely related tumor-associated progression. Elevated PRRX1 connected impact disease progression by modulating transcription. A based demonstrated adverse outcomes, emphasizing importance infiltration clinical intervention strategies. oncology, immunotherapy, reveal mechanisms driving resistance. subtype, linked offers promising target future Emphasizing sensitivity, research highlights strategies life patients.
Language: Английский
Citations
2Biomolecules, Journal Year: 2025, Volume and Issue: 15(2), P. 247 - 247
Published: Feb. 8, 2025
N6-methyladenosine (m6A) is the most prevalent internal chemical modification in eukaryotic messenger RNA (mRNA), significantly impacting its lifecycle through dynamic and reversible processes involving methyltransferase, demethylase, binding proteins. These regulate mRNA stability, splicing, nuclear export, translation, degradation. Programmed cell death (PCD), a tightly controlled process encompassing apoptosis, pyroptosis, ferroptosis, autophagy, necroptosis, plays crucial role maintaining cellular homeostasis, tissue development, function. Recently, m6A has emerged as significant research area due to regulating PCD implications cardiovascular diseases (CVDs). In this review, we delve into intricate relationship between various types modification, emphasizing their pivotal roles initiation progression of CVDs such myocardial ischemia-reperfusion (I/R), atherosclerosis (AS), pulmonary hypertension (PH), cardiomyopathy, doxorubicin (Dox)-induced cardiotoxicity (DIC), heart failure (HF), infarction (MI). Our findings underscore potential elucidating CVD pave new pathways for prevention treatment strategies.
Language: Английский
Citations
2Cell Death and Disease, Journal Year: 2022, Volume and Issue: 13(11)
Published: Nov. 5, 2022
Abstract Heat shock protein (HSP) 90, an important component of the molecular chaperone network, is closely concerned with cellular signaling pathways and stress response by participating in process maturation activation client proteins, playing a crucial role both normal abnormal operation organism. In functionally defective tissues, programmed cell death (PCD) one regulable fundamental mechanisms mediated HSP90, including apoptosis, autophagy, necroptosis, ferroptosis, others. Here, we show complex relationship between HSP90 different types PCD various diseases, discuss possibility as common regulatory nodal multiple PCD, which would provide new perspective for therapeutic approaches disease.
Language: Английский
Citations
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