Mitochondria-Associated Organelle Crosstalk in Myocardial Ischemia/Reperfusion Injury

Journal of Cardiovascular Translational Research, Год журнала: 2024, Номер 17(5), С. 1106 - 1118

Опубликована: Май 28, 2024

Язык: Английский

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Organ-specific model of simulated ischemia/reperfusion and hyperglycemia based on engineered heart tissue

Vascular Pharmacology, Год журнала: 2023, Номер 152, С. 107208 - 107208

Опубликована: Авг. 11, 2023

Here we aimed to establish an in vitro engineered heart tissue (EHT) co-morbidity mimicking model of ischemia-reperfusion injury and diabetes. EHTs were generated from primary neonatal rat cardiomyocytes. Hyperglycemic conditions or hyperosmolar controls applied for one day acute hyperglycemia seven days chronic hyperglycemia. 120 min' simulated ischemia (SI) was followed by reperfusion (R) 1-day follow-up (FR). Normoxic (N) not subjected SI/R. Half the paced, other half left unpaced. To assess cell injury, lactate-dehydrogenase (LDH) concentration measured. Beating force activity (frequency) monitored as cardiomyocyte functional parameters. LDH-release indicated relevant after SI/N each experimental condition, with much higher effects chronically hyperglycemic/hyperosmolar groups. SI stopped beating which returned during reperfusion, weaker recovery than conditions. Acutely treated showed small ∼80% follow-up, while a marked LDH-release, only ∼30% complete loss 24 h reperfusion. We conclude that respond differently SI/R hyperglycemia/hyperosmolarity, our EHT is novel combination diabetes ischemia-reperfusion.

Язык: Английский

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Inhibiting H2AX Can Ameliorate Myocardial Ischemia/Reperfusion Injury by Regulating P53/JNK Signaling Pathway

Cardiology Research and Practice, Год журнала: 2024, Номер 2024(1)

Опубликована: Янв. 1, 2024

Myocardial ischemia‐reperfusion (I/R) injury is a significant area of focus in cardiovascular disease research. I/R can increase intracellular oxidative stress, leading to DNA damage. H2AX plays crucial role repair. This study utilized mouse and cell models myocardial investigate the impact on cardiomyocytes during I/R. initially assessed expression MI/R mice compared sham surgery group. Subsequently, cardiac function, infarct area, mitochondrial damage were evaluated after inhibiting negative control Furthermore, delved into molecular mechanisms by analyzing H2AX, P53, p‐JNK, SHP2, p‐SHP2, p‐RAS, parkin, Drp1, Cyt‐C, Caspase‐3, Caspase‐8 following addition JNK or P53 agonists. The results from western blotting vivo indicated significantly higher group Inhibiting improved reduced mitigated In vitro experiments demonstrated that could attenuate apoptosis cells modulating signaling pathways. These findings suggested may alleviate through regulation P53/JNK pathway, highlighting as potential target for treatment ischemia/reperfusion injury.

Язык: Английский

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Resveratrol inhibits Lin28A expression and induces its degradation via the proteasomal pathway in NCCIT cells

Oncology Letters, Год журнала: 2024, Номер 28(6)

Опубликована: Сен. 30, 2024

Lin28A is an oncoprotein overexpressed in several cancer types such as testicular, ovarian, colon, breast and lung cancers. As a pluripotency factor that promotes tumorigenesis, associated with more undifferentiated aggressive tumors phenotypes. Moreover, highly stable protein difficult to downregulate. The compound resveratrol (RSV) has anticancer effects. present study aimed elucidate the mechanisms underlying downregulation of expression by RSV NCCIT cell line. cells were treated different concentrations investigate its effects on expression. mRNA levels ubiquitin-specific protease 28 (USP28) assessed using reverse transcription-quantitative PCR. Western blot analysis was employed evaluate Lin28A, USP28 phosphorylated Lin28A. In addition, some experiments, MAPK/ERK pathway inhibitor, other experiments involved transfecting small interfering RNAs targeting USP28. results demonstrated significantly reduced destabilizing protein; this effect mediated ability suppress USP28, deubiquitinase normally protects from ubiquitination degradation. Additionally, inhibited phosphorylation via pathway; event previously been shown enhance stability increasing half-life. This resulted degradation through proteasomal cells. provide further evidence activity RSV, identified promising therapeutic targets. oncoprotein, downregulating challenging. However, can overcome hurdle inhibiting signaling promote Furthermore, elucidating these provides avenues for developing targeted therapies.

Язык: Английский

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Progress in Chinese medicine monomers and their nanoformulations on myocardial ischemia/reperfusion injury

Journal of Materials Chemistry B, Год журнала: 2024, Номер unknown

Опубликована: Дек. 4, 2024

The aim of this review is to elucidate the pathomechanism MIRI and present latest developments in use TCM monomers nanomaterials combination with for treatment MIRI.

Язык: Английский

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