Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 26, 2025
Language: Английский
Naunyn-Schmiedeberg s Archives of Pharmacology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 26, 2025
Language: Английский
Coordination Chemistry Reviews, Journal Year: 2024, Volume and Issue: 520, P. 216166 - 216166
Published: Aug. 22, 2024
Language: Английский
Citations
25MedComm, Journal Year: 2024, Volume and Issue: 5(9)
Published: Sept. 1, 2024
Abstract Cell death regulation is essential for tissue homeostasis and its dysregulation often underlies cancer development. Understanding the different pathways of cell can provide novel therapeutic strategies battling cancer. This review explores several key mechanisms apoptosis, necroptosis, autophagic death, ferroptosis, pyroptosis. The research gap addressed involves a thorough analysis how these be precisely targeted therapy, considering tumor heterogeneity adaptation. It delves into genetic epigenetic factors signaling cascades like phosphatidylinositol 3‐kinase/protein kinase B/mammalian target rapamycin (PI3K/AKT/mTOR) mitogen‐activated protein kinase/extracellular signal‐regulated (MAPK/ERK) pathways, which are critical death. Additionally, interaction microenvironment with cells, particularly influence hypoxia, nutrient deprivation, immune cellular interactions, explored. Emphasizing strategies, this highlights emerging modulators inducers such as B lymphoma 2 (BCL2) homology domain 3 (BH3) mimetics, tumour necrosis factor‐related apoptosis‐inducing ligand (TRAIL), chloroquine, innovative approaches to induce ferroptosis provides insights therapy's future direction, focusing on multifaceted circumvent drug resistance. examination evolving underlines considerable clinical potential continuous necessity in‐depth exploration within scientific domain.
Language: Английский
Citations
14Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15
Published: Aug. 20, 2024
Mitochondria play a significant and varied role in inflammatory lung disorders. Mitochondria, known as the powerhouse of cell because their producing energy, are now recognized crucial regulators inflammation immunological responses. Asthma, chronic obstructive pulmonary disease, acute respiratory distress syndrome characterized by complex interactions between immune cells, substances, tissue damage. Dysfunctional mitochondria can increase generation reactive oxygen species (ROS), triggering pathways. Moreover, mitochondrial failure impacts cellular signaling, which turn affects expression molecules that promote inflammation. In addition, have controlling behavior such activation differentiation, is essential development diseases. Their dynamic behavior, encompassing fusion, fission, mitophagy, also responses to oxidative stress. Gaining comprehensive understanding intricate correlation order develop accurate treatment strategies. Targeting ROS generation, dynamics, function may offer novel approaches treating diseases while minimizing Additional investigation into precise contributions will provide knowledge regarding disease mechanisms potential therapeutic approaches. This review focus on how regulate these processes involvement
Language: Английский
Citations
7Cancer Letters, Journal Year: 2024, Volume and Issue: 604, P. 217258 - 217258
Published: Sept. 13, 2024
Language: Английский
Citations
6Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15
Published: Sept. 9, 2024
Ferroptosis is a type of cell death that plays remarkable role in the growth and advancement malignancies including hepatocellular carcinoma (HCC). Non-coding RNAs (ncRNAs) have considerable impact on HCC by functioning as either oncogenes or suppressors. Recent research has demonstrated non-coding ability to control ferroptosis cells, hence impacting tumors resistance these cells drugs. Autophagy mechanism conserved throughout evolution maintaining balance body under normal settings. Nevertheless, occurrence dysregulation autophagy evident progression various human disorders, specifically cancer. dual roles cancer, potentially influencing both survival death. prevalent kind liver genetic mutations changes molecular pathways might worsen its advancement. The subject debate, it capacity repress promote tumor growth. activation can apoptosis, proliferation glucose metabolism, facilitate spread through EMT. Inhibiting hinder enhance respond treatment. regulated several signaling pathways, such STAT3, Wnt, miRNAs, lncRNAs, circRNAs. Utilizing anticancer drugs target may advantageous implications for efficacy cancer
Language: Английский
Citations
5International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 281, P. 136078 - 136078
Published: Sept. 26, 2024
Language: Английский
Citations
4International Journal of Biological Macromolecules, Journal Year: 2024, Volume and Issue: 282, P. 136891 - 136891
Published: Oct. 28, 2024
Language: Английский
Citations
4Microchemical Journal, Journal Year: 2025, Volume and Issue: unknown, P. 112640 - 112640
Published: Jan. 1, 2025
Language: Английский
Citations
0Deleted Journal, Journal Year: 2025, Volume and Issue: unknown, P. 100029 - 100029
Published: Jan. 1, 2025
Language: Английский
Citations
0Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)
Published: Jan. 17, 2025
Sepsis is a systemic inflammatory syndrome that can cause coagulation abnormalities, leading to damage in multiple organs. Vascular endothelial cells (VECs) are crucial the development of sepsis-induced coagulopathy (SIC). The role Parthenolide (PTL) regulating SIC by protecting VECs remains unclear. study utilized septic rats and lipopolysaccharide (LPS)-stimulated simulate model observe therapeutic effects PTL. Additionally, nanotechnology was employed produce Nano-PTL (N-PTL), whether it has advantages over PTL treating SIC. been shown mitigate lung injury rats, significantly reduce tumor necrosis factor-α (TNF-α) levels, increase survival rates. treatment also enhances function, augments vascular cell (VEC) reduces mitochondrial fragmentation, increases both oxygen consumption rate (OCR) membrane potential (MMP), while inhibiting reactive species (ROS) production. By increasing BRD4/BCL-xL prevent mitochondrial-mediated apoptosis VECs, improve VEC consequently ameliorate nanotechnology-synthesized N-PTL further protective on function. This clarifies mechanisms SIC, offering new strategies directions for sepsis.
Language: Английский
Citations
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