Radiotherapy promotes cuproptosis and synergizes with cuproptosis inducers to overcome tumor radioresistance

Cancer Cell, Год журнала: 2025, Номер unknown

Опубликована: Апрель 1, 2025

Язык: Английский

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LncRNA‐MEG3 Regulates Muscle Mass and Metabolic Homeostasis by Facilitating SUZ12 Liquid–Liquid Phase Separation

Advanced Science, Год журнала: 2025, Номер unknown

Опубликована: Апрель 26, 2025

Abstract Skeletal muscle plays a crucial role in maintaining motor function and metabolic homeostasis, with its loss or atrophy leading to significant health consequences. Long non‐coding RNAs (lncRNAs) have emerged as key regulators biology; however, their precise roles pathology remain be fully elucidated. This study demonstrates that lncRNA maternally expressed gene 3 (MEG3) is preferentially slow‐twitch fibers dynamically regulated during development, aging, the context of Duchenne muscular dystrophy (DMD). Using both loss‐ gain‐of‐function mice models, this shows lncRNA‐MEG3 critical for preserving mass function. Its depletion leads atrophy, mitochondrial dysfunction, impaired regenerative capacity, while overexpression enhances mass, increases oxidative fiber content, improves endurance. Notably, MDX significantly alleviates wasting adipose tissue infiltration. Mechanistically, uncovers novel interaction between polycomb repressive complex 2 (PRC2), where binds SUZ12 subunit (Suz12), stabilizes PRC2, facilitates liquid–liquid phase separation (LLPS), regulates epigenetic modulation four half lim domains (Fhl3) ring finger protein 128 (Rnf128). These findings not only highlight homeostasis but also provide new insights into lncRNA‐based therapeutic strategies muscle‐related diseases.

Язык: Английский

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Apelin deficiency exacerbates cardiac injury following infarction by accelerating cardiomyocyte ferroptosis

Free Radical Research, Год журнала: 2024, Номер unknown, С. 1 - 14

Опубликована: Дек. 28, 2024

Apelin is an endogenous ligand for the receptor and a critical protective effector in myocardial infarction (MI). Nevertheless, these mechanisms are not fully understood. Ferroptosis major driving factor of MI. This study aimed to investigate effects underlying regulatory on cardiomyocyte ferroptosis A model MI was induced adult C57BL/6J wild type (WT) knockout (Apelin−/−) mice. Cardiac function examined by echocardiography 4 weeks post-MI. RNA-seq, histochemical analyses, Western blotting were applied examine transcriptome pathological remodeling following molecular mechanisms. Mice neonatal cardiomyocytes (NCMs) used establish serum deprivation/hypoxia (SD/H) vitro. Compared with WT mice, Apelin−/− mice exhibited more severe impairment cardiac increased fibrosis infarction. Transcriptome biochemical analyses revealed involvement mediating Ferroptosis-related proteins significantly post-MI whereas p-AMPK greatly decreased. treatment activated AMPK pathway thereby inhibited NCMs SD/H These partially reversed inhibitor. deficiency aggravated dysfunction activating via inhibition pathway. offers novel potential therapeutic target treatment.

Язык: Английский

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Feasibility and Safety of Targeting Mitochondria Function and Metabolism in Acute Myeloid Leukemia

Current Pharmacology Reports, Год журнала: 2024, Номер unknown

Опубликована: Окт. 4, 2024

Язык: Английский

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