Autophagy and Programmed Cell Death Modalities Interplay in HIV Pathogenesis

Cells, Journal Year: 2025, Volume and Issue: 14(5), P. 351 - 351

Published: Feb. 28, 2025

Human immunodeficiency virus (HIV) infection continues to be a major global health challenge, affecting 38.4 million according the Joint United Nations Program on HIV/AIDS (UNAIDS) at end of 2021 with 1.5 new infections. New HIV infections increased during 2 years after COVID-19 pandemic. Understanding intricate cellular processes underlying pathogenesis is crucial for developing effective therapeutic strategies. Among these processes, autophagy and programmed cell death modalities, including apoptosis, necroptosis, pyroptosis, ferroptosis, play pivotal roles in host-virus interaction dynamics. Autophagy, highly conserved mechanism, acts as double-edged sword infection, influencing viral replication, immune response modulation, fate infected cells. Conversely, critical defense mechanism against spread contributes depletion CD4+ T cells, hallmark progression. This review aims dissect complex interplay between modalities HIV-induced pathogenesis. It highlights molecular mechanisms involved, their persistence dysfunction, challenges posed by reservoir drug resistance, which continue impede management pathology. Targeting pathways holds promise novel strategies mitigate chronic inflammation, ultimately improving outcomes individuals living HIV.

Language: Английский

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Exploring the Role of Metabolic Hyperferritinaemia (MHF) in Steatotic Liver Disease (SLD) and Hepatocellular Carcinoma (HCC)

Cancers, Journal Year: 2025, Volume and Issue: 17(5), P. 842 - 842

Published: Feb. 28, 2025

The increasing prevalence of the spectrum Steatotic Liver Disease (SLD), including Metabolic-Associated (MASLD), Steatohepatitis (MASH), and progression to Cirrhosis Hepatocellular Carcinoma (HCC) has led intense research in disease pathophysiology, with many studies focusing on role iron. Iron overload, which is often observed patients SLD as a part metabolic hyperferritinaemia (MHF), particularly reticuloendothelial system (RES), can exacerbate steatosis. This imbalance iron distribution, coupled high-fat diet, further promote by means oxidative stress triggering inflammation activating hepatic stellate cells (HSCs), therefore leading fibrosis simple steatosis more severe MASH. influence overload also been shown complex ferroptosis, type cell death driven iron-dependent lipid peroxidation. Ferroptosis depletes liver's antioxidant capacity, contributing development MASH, while its MASH-related HCC potentially linked alternations tumour microenvironment, well ferroptosis resistance. iron-rich steatotic environment becomes prone hepatocarcinogenesis activation several pro-carcinogenic mechanisms epithelial-to-mesenchymal transition deactivation DNA damage repair. Biochemical markers deranged metabolism have all stages associated multiple patient cohorts diverse genetic backgrounds, enhancing our daily clinical understanding this interaction. Further could lead enhanced therapies for management prevention.

Language: Английский

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Pulling back the mitochondria’s iron curtain

npj Metabolic Health and Disease, Journal Year: 2025, Volume and Issue: 3(1)

Published: March 4, 2025

Language: Английский

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Role of liensinine in sensitivity of activated macrophages to ferroptosis and in acute liver injury

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

Published: June 23, 2023

Acute liver injury (ALI) is an acute inflammatory disease with a high mortality rate. Alternatively, activated macrophages (AAMs) have been linked to the inflammation and recovery of ALI. However, mechanism underlying AAM death in ALI has not studied sufficiently. We used liensinine (Lie) as drug choice after screening library small-molecule monomers 1488 compounds from traditional Chinese remedies. In ALI, we evaluated potential therapeutic effects mechanisms action found that it effectively inhibited RSL3-induced ferroptosis AAM. Lie significantly reduced lipid peroxidation RSL3-generated It also improved survival rate LPS/D-GalN-treated mice, serum transaminase activity, suppressed factor production, may lowered ferritinophagy blocked Fe2+ synthesis. Following combined treatment RSL3 Lie, super-resolution microscopy revealed close correlation between ferritin LC3-positive vesicles The co-localization LC3 LAMP1 was reduced. These findings suggest ameliorate by inhibiting enhancing AMM resistance autophagosome-lysosome fusion. Therefore, be agent for patients

Language: Английский

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靶向铁死亡和铁自噬: 心血管疾病的新靶点?

Journal of Zhejiang University SCIENCE B, Journal Year: 2024, Volume and Issue: 25(1), P. 1 - 22

Published: Jan. 1, 2024

Language: Английский

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