SIRT6 mitigates doxorubicin-induced cardiomyopathy via amelioration of mitochondrial dysfunction: A mechanistic study implicating the activation of the Nrf-2/FUNDC1 signaling axis DOI Creative Commons
Qi Wang, Hongshuo Shi,

Haowen Zhuang

и другие.

International Journal of Medical Sciences, Год журнала: 2025, Номер 22(7), С. 1640 - 1657

Опубликована: Фев. 28, 2025

Doxorubicin-induced myocardial injury, characterized by hypertrophy and heart failure (HF), represents a primary contributor to end-stage cardiovascular mortality associated with anthracycline drugs. Prior research has elucidated that SIRT6-mediated oxidative processes mitochondrial metabolic reprogramming are pivotal in sustaining energy metabolism during damage cardiomyocytes. In the aftermath of doxorubicin-induced fibrosis exacerbate impairment cardiac ejection function, resulting elevated oxygen consumption. This condition is accompanied disrupted ATP production, diminished biogenesis, inadequate synthesis new DNA, collectively triggering necroptosis apoptosis pathways. Our preliminary experimental results have confirmed SIRT6, traditional medicine, exerts cardioprotective effects. Nevertheless, interaction between SIRT6 Nrf-2-mediated biogenesis context HF remains inadequately understood. The generation mitochondria key mechanism involved DNA repair cell cycle management.

Язык: Английский

Emerging insights into the pathogenesis and therapeutic strategies for vascular endothelial injury-associated diseases: focus on mitochondrial dysfunction DOI Creative Commons
Boxian Pang, Guangtong Dong,

Tieliang Pang

и другие.

Angiogenesis, Год журнала: 2024, Номер 27(4), С. 623 - 639

Опубликована: Июль 26, 2024

Abstract As a vital component of blood vessels, endothelial cells play key role in maintaining overall physiological function by residing between circulating and semi-solid tissue. Various stress stimuli can induce injury, leading to the onset corresponding diseases body. In recent years, importance mitochondria vascular injury has become increasingly apparent. Mitochondria, as primary site cellular aerobic respiration organelle for “energy information transfer,” detect cell damage integrating receiving various external signals. The generation reactive oxygen species (ROS) mitochondrial dysfunction often determine evolution towards necrosis or apoptosis. Therefore, are closely associated with function, helping progression clinical diseases. This article comprehensively reviews interconnection pathogenesis mitochondrial-induced cardiovascular diseases, renal pulmonary-related cerebrovascular microvascular diabetes. Corresponding therapeutic approaches also provided. Additionally, strategies using drugs treat injury-based discussed, aiming offer new insights treatment options diagnosis related injuries.

Язык: Английский

Процитировано

44
Ginsenoside Rb1 ameliorates heart failure through DUSP-1-TMBIM-6-mediated mitochondrial quality control and gut flora interactions DOI

Xiangyi Pu,

Qin Zhang, Jinfeng Liu

и другие.

Phytomedicine, Год журнала: 2024, Номер 132, С. 155880 - 155880

Опубликована: Июль 20, 2024

Язык: Английский

Процитировано

30
Exploring the Mechanism of Ferroptosis Induction by Sappanone A in Cancer: Insights into the Mitochondrial Dysfunction Mediated by NRF2/xCT/GPX4 Axis DOI Creative Commons

Junyan Wang,

Haowen Zhuang,

Xiaocui Yang

и другие.

International Journal of Biological Sciences, Год журнала: 2024, Номер 20(13), С. 5145 - 5161

Опубликована: Янв. 1, 2024

Non-small cell lung cancer (NSCLC), a major subtype of cancer, encompasses squamous carcinoma, adenocarcinoma, and large carcinoma. Compared to small NSCLC cells grow divide more slowly, their metastasis occurs at later stage. Currently, chemotherapy is the primary treatment for this disease. Sappanone A (SA) flavonoid compound extracted from plant Caesalpinia sappan, known its antitumor, redox-regulating, anti-inflammatory properties. Recent studies have investigated interaction SA with mitochondrial pathways in regulating death through Nrf-2/GPX-4/xCT axis. This study specifically explores mechanism by which affects morphology structure regulation mitophagy biogenesis tumor cells. The primarily utilizes second-generation transcriptomic sequencing data molecular docking techniques elucidate role programmed omics results indicate that significantly targets genes involved oxidative phosphorylation, mitophagy, dynamics, stress. Further findings confirmed Nrf-2/GPX4/xCT pathway serves as crucial target NSCLC. Knockdown Nrf-2 (si-Nrf-2) overexpression (ad-Nrf-2) were shown modulate therapeutic efficacy varying degrees. Additionally, modifications GPX4/xCT affected regulatory effects on autophagy, biogenesis, energy metabolism. These mechanisms may be mediated caspase ferroptosis-related signaling. Molecular biology experiments demonstrated intervention further inhibits phosphorylation FUNDC1 Tyr18 downregulates TOM20 expression. was found reduce expression PGC1α, Nrf-1, Tfam, resulting decrease respiration Overexpression counteract biogenesis. Confocal microscopy revealed increases fragmentation, subsequently inducing pathway-mediated death. However, genetic modification altered In conclusion, has been identified promising agent apoptosis ferroptosis represent key Targeting axis offers novel approach maintaining homeostasis within cellular microenvironment.

Язык: Английский

Процитировано

22
Mitochondrial diseases: from molecular mechanisms to therapeutic advances DOI Creative Commons
Hu Wen,

Hui Deng,

Bingyan Li

и другие.

Signal Transduction and Targeted Therapy, Год журнала: 2025, Номер 10(1)

Опубликована: Янв. 9, 2025

Abstract Mitochondria are essential for cellular function and viability, serving as central hubs of metabolism signaling. They possess various metabolic quality control mechanisms crucial maintaining normal activities. Mitochondrial genetic disorders can arise from a wide range mutations in either mitochondrial or nuclear DNA, which encode proteins other contents. These defects lead to breakdown metabolism, such the collapse oxidative phosphorylation, one mitochondria’s most critical functions. diseases, common group disorders, characterized by significant phenotypic heterogeneity. Clinical symptoms manifest systems organs throughout body, with differing degrees forms severity. The complexity relationship between mitochondria diseases results an inadequate understanding genotype-phenotype correlation these historically making diagnosis treatment challenging often leading unsatisfactory clinical outcomes. However, recent advancements research technology have significantly improved our management conditions. translations mitochondria-related therapies actively progressing. This review focuses on physiological mitochondria, pathogenesis potential diagnostic therapeutic applications. Additionally, this discusses future perspectives diseases.

Язык: Английский

Процитировано

11
Astragaloside IV alleviates septic myocardial injury through DUSP1-Prohibitin 2 mediated mitochondrial quality control and ER-autophagy DOI Creative Commons
Junyan Wang,

Xiangyi Pu,

Haowen Zhuang

и другие.

Journal of Advanced Research, Год журнала: 2024, Номер unknown

Опубликована: Ноя. 1, 2024

Septic cardiomyopathy (SCM) is a complication of myocardial injury in patients with severe sepsis. This study highlights the potential Astragaloside IV(AS) treatment septic and provides reference for developing cardioprotective drugs targeting DUSP1-PHB2-related mitochondria-ER interaction. Dual specificity phosphatase-1 (DUSP1)/Prohibitin 2 cardiomyocyte-specific knockout mice (DUSP1/PHB2CKO) /DUSP1 transgenic (DUSP1/PHB2TG) were used to generate LPS-induced sepsis models. The pathological mechanism by which AS-IV improves heart was detected using cardiac ultrasound, fluorescence staining, transmission electron microscopy, western blotting. After siRNA cardiomyocytes DUSP-1/PHB2, changes mitochondrial function morphology determined qPCR, blotting, ELISA, laser confocal targeted therapeutic effects further examined. SCM leads dysfunction. However, IV (AS) normalizes homeostasis ER function. Notably, protective effect blocked DUSP1/Prohibitin but remained unaffected DUSP1 (DUSP1/PHB2TG). AS DUSP1-PHB2 related

Язык: Английский

Процитировано

10
Mitochondrial Dysfunction in Endothelial Cells: A Key Driver of Organ Disorders and Aging DOI Creative Commons
Elena Grossini, Sakthipriyan Venkatesan, Mohammad Mostafa Ola Pour

и другие.

Antioxidants, Год журнала: 2025, Номер 14(4), С. 372 - 372

Опубликована: Март 21, 2025

Mitochondria are of great importance in cell biology since they major sites adenosine triphosphate (ATP) production and widely involved different cellular pathways the response to stress. During ATP production, reactive oxygen species (ROS) can be produced. While a small amount ROS may important for regulation physiological processes, at elevated levels turn into harmful agents leading damage. From pathological perspective, it could particularly interesting focus on mitochondrial function endothelial cells development aging onset diseases, including renal, cardio-metabolic, liver neurodegenerative ones. However, date, there no surveys which address above issues. To fill this gap, valuable collect recent findings about role mitochondria function, not only increase knowledge but also clinical applications. Here, we overview most issues view characterizing as an innovative potential target prevention aging, well treatment conditions.

Язык: Английский

Процитировано

2
Spermine alleviates myocardial cell aging by inhibiting mitochondrial oxidative stress damage DOI

Jing Yang,

Chunrui Zhang, Zixuan Li

и другие.

European Journal of Pharmacology, Год журнала: 2025, Номер unknown, С. 177477 - 177477

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

1
Flavonoids in the regulation of microglial-mediated neuroinflammation; focus on fisetin, rutin, and quercetin DOI

Mohannad Hamid Jasim,

Rosull Saadoon Abbood,

Gaurav Sanghvi

и другие.

Experimental Cell Research, Год журнала: 2025, Номер unknown, С. 114537 - 114537

Опубликована: Март 1, 2025

Язык: Английский

Процитировано

1
MiR-718-mediated inhibition of prohibitin 1 influences mitochondrial dynamics, proliferation, and migration of keratinocytes DOI

Himani Rani,

Neeru Saini

Mitochondrion, Год журнала: 2025, Номер unknown, С. 102041 - 102041

Опубликована: Апрель 1, 2025

Язык: Английский

Процитировано

1
The Role of Autophagy in Vascular Endothelial Cell Health and Physiology DOI Creative Commons

Meghan Hu,

Joseph M. Ladowski, He Xu

и другие.

Cells, Год журнала: 2024, Номер 13(10), С. 825 - 825

Опубликована: Май 11, 2024

Autophagy is a highly conserved cellular recycling process which enables eukaryotes to maintain both and overall homeostasis through the catabolic breakdown of intracellular components or selective degradation damaged organelles. In recent years, importance autophagy in vascular endothelial cells (ECs) has been increasingly recognized, numerous studies have linked dysregulation development dysfunction disease. Here, we provide an overview molecular mechanisms underlying ECs our current understanding roles biology review implications dysregulated for Finally, summarize state research on compounds modulate identify challenges their translation into clinical use.

Язык: Английский

Процитировано

5