International Immunopharmacology, Год журнала: 2024, Номер 144, С. 113722 - 113722
Опубликована: Дек. 1, 2024
Язык: Английский
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
2
Frontiers in Physiology, Год журнала: 2024, Номер 15
Опубликована: Янв. 29, 2024
Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, maintain cellular homeostasis by removing damaged mitochondria participating developing diseases. Research has confirmed exercise regulate mitophagy levels, thereby exerting protective effects This article reviews role of diseases, on mitophagy, potential mechanisms exercise-regulated intervention providing new insights for future basic clinical research interventions to prevent treat
Язык: Английский
Процитировано
8
Phytomedicine, Год журнала: 2024, Номер 126, С. 155441 - 155441
Опубликована: Фев. 10, 2024
The mitochondrial unfolded protein response (UPRmt) is the first line of defense against dysfunction in several diseases. Baicalein, which an extract Scutellaria baicalensis Georgi roots, exerts mitoprotective effects on metabolic disorders and cardiovascular However, it remains unclear whether baicalein alleviates obesity-induced cardiac damage through UPRmt. present research designed to clarify role lipotoxicity-induced myocardial apoptosis investigated UPRmt-related mechanism. In vitro experiment, palmitic acid (PA)-treated AC16 cardiomyocytes were established mimic injury. After pretreatment cells with baicalein, levels cell vitality, apoptosis, membrane potential, oxidative stress, proteins determined. Additionally, treated ML385 or siRNA explore regulation UPRmt by NRF2 signaling. vivo male db/db mice administered for 8 weeks used validate induced obesity, UPRmt, NRF2-related pathway. cardiomyocytes, PA dose-dependently increased expression markers (HSP60, LONP1, ATF4, ATF5). This increase was accompanied enhanced production ROS, reduced elevated cytochrome c, cleaved caspase-3, Bax/Bcl2, eventually leading apoptosis. Baicalein treatment reversed activation impeded mitochondrial-mediated Moreover, downregulation its inhibitor diminished baicalein-mediated signaling inhibition triggered dysfunction. deficiency more intensely activated resulting stress PA-induced thus indicating that plays a vital homeostasis regulation. study mice, inhibited antioxidant capacity, attenuated NRF2-activated To our best knowledge, these results provide insight inhibits induce protective effect cardiomyocyte via activating suggest new
Язык: Английский
Процитировано
8
International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(17), С. 13472 - 13472
Опубликована: Авг. 30, 2023
Molecular oxygen (O2) is one of the four most important elements on Earth (alongside carbon, nitrogen and hydrogen); aerobic organisms depend it to release energy from carbon-based molecules [...].
Язык: Английский
Процитировано
13
Phytomedicine, Год журнала: 2024, Номер 133, С. 155894 - 155894
Опубликована: Июль 20, 2024
Язык: Английский
Процитировано
5
International Journal of Medical Sciences, Год журнала: 2024, Номер 21(13), С. 2502 - 2509
Опубликована: Янв. 1, 2024
Hypoxic injury is a critical pathological factor in the development of various cardiovascular diseases, such as congenital heart disease, myocardial infarction, and failure. Mitochondrial quality control essential for protecting cardiomyocytes from hypoxic damage. Under conditions, disruptions mitochondrial homeostasis result excessive reactive oxygen species (ROS) production, imbalances dynamics, initiate processes including oxidative stress, inflammatory responses, apoptosis. Targeted interventions to enhance control, coenzyme Q10 statins, have shown promise mitigating hypoxia-induced dysfunction. These treatments offer potential therapeutic strategies hypoxia-related diseases by regulating fission fusion, restoring biogenesis, reducing ROS promoting mitophagy.
Язык: Английский
Процитировано
5
ONCOLOGIE, Год журнала: 2025, Номер unknown
Опубликована: Март 17, 2025
Язык: Английский
Процитировано
0
Journal of Translational Medicine, Год журнала: 2025, Номер 23(1)
Опубликована: Апрель 10, 2025
Acute myocardial infarction (AMI) and the ischemia-reperfusion injury (MI/RI) that typically ensues represent a significant global health burden, accounting for considerable number of deaths disabilities. In context AMI, percutaneous coronary intervention (PCI) is preferred treatment option reducing acute ischemic damage to heart. Despite modernity PCI therapy, pathological cardiomyocytes due MI/RI remains an important target affects long-term prognosis patients. recent years, mitochondrial dysfunction during AMI has been increasingly recognized as critical factor in cardiomyocyte death. Damaged mitochondria play active role formation inflammatory environment by triggering key signaling pathways, including those mediated cyclic GMP-AMP synthase, NOD-like receptors Toll-like receptors. This review emphasizes dual both contributors regulators inflammation. The aim explore complex mechanisms its profound impact on immune dysregulation. Specific interventions mitochondrial-targeted antioxidants, membrane-stabilizing peptides, transplantation therapies have demonstrated efficacy preclinical models.
Язык: Английский
Процитировано
0
Frontiers in Pharmacology, Год журнала: 2024, Номер 15
Опубликована: Март 20, 2024
Significant advances in chemotherapy drugs have reduced mortality patients with malignant tumors. However, chemotherapy-related cardiotoxicity increases the morbidity and of patients, has become second leading cause death after tumor recurrence, which received more attention recent years. Arrhythmia is one common types chemotherapy-induced cardiotoxicity, a new risk related to treatment, seriously affects therapeutic outcome patients. Traditional Chinese medicine experienced thousands years clinical practice China, accumulated wealth medical theories treatment formulas, unique advantages prevention diseases. may reduce arrhythmic toxicity caused by without affecting anti-cancer effect. This paper mainly discussed pathogenesis secondary chemotherapeutic drug-induced arrhythmia (CDIA), summarized studies on compounds, Combination Formula injection that be beneficial intervention CDIA including atrial fibrillation, ventricular sinus bradycardia, order provide reference for arrhythmias.
Язык: Английский
Процитировано
4
Current Pharmaceutical Design, Год журнала: 2024, Номер 30(13), С. 969 - 974
Опубликована: Март 29, 2024
Abstract: In metabolic syndrome and diabetes, compromised mitochondrial function emerges as a critical driver of cardiovascular disease, fueling its development persistence, culminating in cardiac remodeling adverse events. this context, angiotensin II - the main interlocutor renin-angiotensin-aldosterone system promotes local systemic oxidative inflammatory processes. To highlight, low activity/expression proteins called sirtuins negatively participates these processes, allowing more significant imbalance, which impacts cellular tissue responses, causing damage, inflammation, vascular remodeling. The reduction energy production mitochondria has been widely described element all types disorders. Additionally, high sirtuin levels AMPK signaling stimulate hypoxia-inducible factor 1 beta promote ketonemia. Consequently, enhanced autophagy mitophagy advance through cells, sweeping away debris silencing orchestra stress ultimately protecting vulnerable from damage. highlight particular interest, SGLT2 inhibitors (SGLT2i) profoundly influence mechanisms. Randomized clinical trials have evidenced compelling picture SGLT2i emerging game-changers, wielding their power to demonstrably improve slash rates renal Furthermore, driven by recent evidence, emerge supermolecules, exerting beneficial actions increase efficiency, alleviate stress, curb severe inflammation. Its strengthen tissues create resilient defense against disease. conclusion, like treasure chest brimming with untold riches, on holds potential for health. Unlocking secrets, map guiding adventurers hidden promises pave way even potent therapeutic strategies.
Язык: Английский
Процитировано
4