Mangiferin Promotes Porcine Oocyte Maturation and Delays the Postovulatory Aging Process by Up-Regulating Nrf2 Levels DOI

X-M Yuan,

Hongchao Ji, Yuhao Zhang

и другие.

Опубликована: Янв. 1, 2024

Язык: Английский

Nuclear receptor subfamily 4 group A member 1 promotes myocardial ischemia/reperfusion injury through inducing mitochondrial fission factor-mediated mitochondrial fragmentation and inhibiting FUN14 domain containing 1-depedent mitophagy DOI Creative Commons
Junyan Wang,

Haowen Zhuang,

Lianqun Jia

и другие.

International Journal of Biological Sciences, Год журнала: 2024, Номер 20(11), С. 4458 - 4475

Опубликована: Янв. 1, 2024

This study investigated the mechanism by which NR4A1 regulates mitochondrial fission factor (Mff)-related and FUN14 domain 1 (FUNDC1)-mediated mitophagy following cardiac ischemia-reperfusion injury(I/R). Our findings showed that damage regulation was positively correlated with pathological pan-apoptosis of myocardial cell mitochondria. Compared wild-type mice (WT), NR4A1-knockout exhibited resistance to injury fission, characterized activation. Results increased expression level, activating mediated Mff restoring phenotype FUNDC1. The inactivation FUNDC1 phosphorylation could not mediate normalization in a timely manner, leading an excessive stress response unfolded proteins imbalance homeostasis. process disrupted quality control network, accumulation damaged mitochondria activation pan-apoptotic programs. data indicate is novel critical target I/R exertsand negative regulatory effects Mff-mediated mito-fission inhibiting FUNDC1-mediated mitophagy. Targeting crosstalk balance between NR4A1-Mff-FUNDC1 potential approach for treating I/R.

Язык: Английский

Процитировано

22

Assisted Reproduction Technologies (ART): Impact of Mitochondrial (Dys)function and Antioxidant Therapy DOI Creative Commons
Filipa C. Ferreira, José Teixeira,

Fernando José Cebola Lidon

и другие.

Animals, Год журнала: 2025, Номер 15(3), С. 289 - 289

Опубликована: Янв. 21, 2025

In the last decades, major changes in ecosystems related to industrial development and environmental modifications have had a direct impact on mammalian fertility, as well biodiversity. It is widely demonstrated that all these impair reproductive function. Several studies connected increase of reactive oxygen species (ROS) generated mitochondria recently identified decline fertility due various factors, including heat stress. The study antioxidants, especially targeted has been focused identifying more efficient less toxic therapies could circumvent problems. These antioxidants can be derived from natural compounds diet delivered effective forms, providing much therapy. use mitochondriotropic diet-based assisted technologies (ART) may an important way overcome low allowing conservation animal biodiversity productivity. This paper provides concise review current state art this topic, with particular focus mitoquinone, AntiOxBEN2, AntiOxCIN4, urolithin A piperine, their effects bovine other species.

Язык: Английский

Процитировано

1

GPD1L‐Mediated Glycerophospholipid Metabolism Dysfunction in Women With Diminished Ovarian Reserve: Insights From Pseudotargeted Metabolomic Analysis of Follicular Fluid DOI Creative Commons
Jiaqi Wu,

Xuehan Zhao,

Ying Fang

и другие.

Cell Proliferation, Год журнала: 2025, Номер unknown

Опубликована: Март 20, 2025

ABSTRACT Diminished ovarian reserve (DOR) is a pathological condition characterised by reduced function, which refers to the decreased quality and quantity of oocytes, potentially causing female infertility various health issues. Follicular fluid (FF) serves as microenvironment for follicular development oocyte maturation, gaining an in‐depth understanding metabolic state FF will help us uncover key biological processes involved in aging, while specific underlying pathogenic mechanisms are not fully understood. In this study, we utilised pseudotargeted metabolomic analysis reveal glycerophospholipid metabolism dysfunction mediated GPD1L DOR patients. We also found that was downregulated granulosa cells (GCs) patients, resulting increased cell apoptosis mitochondrial dysfunction. Moreover, our results demonstrated expression could induce atresia impair mouse ovaries. Altogether, research suggested GCs metabolites pathway act novel biomarkers diagnosis, paving way new theoretical basis pathogenesis DOR.

Язык: Английский

Процитировано

1

Emerging therapeutic strategies to mitigate female and male reproductive aging DOI
Yasmyn E. Winstanley, Jennifer Stables, Macarena B. Gonzalez

и другие.

Nature Aging, Год журнала: 2024, Номер 4(12), С. 1682 - 1696

Опубликована: Дек. 13, 2024

Язык: Английский

Процитировано

5

Interleukins‐27 Aggravates Liver Injury by Impairing the Antimicrobial Response of Macrophages via the Promotion of Mitochondrial Dysfunction in the Context of Sepsis DOI Creative Commons
Yuehua You, Yuyan Li, Lin Ye

и другие.

Mediators of Inflammation, Год журнала: 2025, Номер 2025(1)

Опубликована: Янв. 1, 2025

Background and Aims: Plasma interleukin (IL)-27 is an important mediator of acute hepatic injury (AHI) associated with sepsis. Mitochondria contribute to the proper regulation macrophage phagocytosis. In this study, we investigated effect IL-27 on mitochondrial function antimicrobial response macrophages in sepsis-associated AHI. Methods: Wild-type (WT) receptor WSX-1 deficient (IL-27R-/-) mice underwent cecal ligation puncture (CLP). The severity injury, inflammatory cytokine levels, pyroptosis, bacterial load liver blood were assessed 24 h after CLP. vitro, RAW264.7 cells peritoneal treated lipopolysaccharide (LPS) and/or IL-27. phagocytosis killing functions detected. Mitochondrial mitophagy detected using western blot, glutathione (GSH)/malondialdehyde (MDA) content measurement, fluorescence staining, JC-1 staining vivo vitro. After treatment nicotinamide mononucleotide (NMN, NAD + precursor), a pharmacologic agent that improves function, response, pyroptosis assessed. Results: IL-27R-/- exhibited marked reduction (based cleaved GSDMD Caspases 1 protein levels), systemic inflammation serum IL-6, IL-10, TNF-α levels) compared WT following CLP, lacking IL-27R displayed significantly higher clearance greater local infection control. Subsequent studies demonstrated directly impaired LPS-induced phagocytosis, capacity, macrophages. Finally, enhanced NMN alleviated pathological inflammation. Conclusions: These findings indicated impairs capacity by aggravating dysfunction aggravate AHI during

Язык: Английский

Процитировано

0

Mangiferin promotes porcine oocyte maturation and delays the postovulatory aging process by up-regulating NRF2 levels DOI

Xiu‐Wen Yuan,

Hongchao Ji, Yuhao Zhang

и другие.

Theriogenology, Год журнала: 2025, Номер 239, С. 117384 - 117384

Опубликована: Март 10, 2025

Язык: Английский

Процитировано

0

The Importance of Mitochondrial Processes in the Maturation and Acquisition of Competences of Oocytes and Embryo Culture DOI Open Access
Elżbieta Gałęska, Alicja Kowalczyk, Marcjanna Wrzecińska

и другие.

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(9), С. 4098 - 4098

Опубликована: Апрель 25, 2025

Mitochondria, as multifunctional and partially independent structures, play a crucial role in determining essential life processes. Recently, their significance reproductive biology has gained increasing attention. This review aims to comprehensively analyse the of mitochondrial processes oocyte maturation embryo culture. A comprehensive literature was conducted highlight importance activity early stages formation. Proper function provides energy, maintains genomic stability, ensures optimal conditions for fertilisation progression. Understanding these is optimise culture identify new biomarkers that improve success assisted technologies (ARTs). Enhancing female cells key improving quality, which can lead better vitro transfer. Furthermore, advances diagnostic techniques, such genome sequencing, offer more precise understanding relationship between health quality. However, fully functions only part challenge. Expanding knowledge interactions mitochondria other cellular structures future advancements medicine. complex relationships will provide deeper insight into outcomes development.

Язык: Английский

Процитировано

0

Assisted Reproductive Technology: A Ray of Hope for Infertility DOI Creative Commons
Rumiana Koynova, Qiongqiong Angela Zhou

ACS Omega, Год журнала: 2025, Номер unknown

Опубликована: Май 23, 2025

Язык: Английский

Процитировано

0

Mitochondrial Dysfunction: The Silent Catalyst of Kidney Disease Progression DOI Creative Commons
Nikola Pavlović,

Marinela Križanac,

Marko Kumrić

и другие.

Cells, Год журнала: 2025, Номер 14(11), С. 794 - 794

Опубликована: Май 28, 2025

Mitochondrial dysfunction is a pivotal driver in the pathogenesis of acute kidney injury (AKI), chronic disease (CKD), and congenital anomalies urinary tract (CAKUT). The kidneys, second only to heart mitochondrial density, rely on oxidative phosphorylation meet high ATP demands solute reabsorption filtration. Disrupted dynamics, such as excessive fission mediated by Drp1, exacerbate tubular apoptosis inflammation AKI models like ischemia–reperfusion injury. In CKD, persistent drives stress, fibrosis, metabolic reprogramming, with epigenetic mechanisms (DNA methylation, histone modifications, non-coding RNAs) regulating genes critical for homeostasis, PMPCB TFAM. Epigenetic dysregulation also impacts mitochondrial–ER crosstalk, influencing calcium signaling autophagy renal pathology. Mitophagy, selective clearance damaged mitochondria, plays dual role disease. While PINK1/Parkin-mediated mitophagy protects against cisplatin-induced preventing fragmentation apoptosis, its contributes fibrosis CKD progression. For instance, macrophage-specific loss regulators MFN2 amplifies ROS production fibrotic responses. Conversely, BNIP3/NIX-dependent attenuates contrast-induced suppressing NLRP3 inflammasome activation. diabetic nephropathy, impaired correlates declining eGFR interstitial highlighting diagnostic therapeutic potential. Emerging strategies target through antioxidants (e.g., MitoQ, SS-31), inducers COPT nanoparticles), transplantation, which mitigates restoring bioenergetics modulating inflammatory pathways. Nanotechnology-enhanced drug delivery systems, curcumin-loaded nanoparticles, improve targeting reduce stress. interventions, including PPAR-α agonists KLF4 modulators, show promise reversing reprogramming fibrosis. These advances underscore mitochondria central hubs pathophysiology. Tailored interventions—ranging from Drp1 inhibition transplantation—hold transformative potential mitigate clinical outcomes. Additionally, dietary interventions novel adenogens are emerging promising modulate function attenuate Future research should address gaps understanding CAKUT optimize targeted systems precision therapies.

Язык: Английский

Процитировано

0

Mitochondrial dysfunction in pregnancy loss: a review DOI

Lingjing Lu,

Xinyue Huang,

Yuqian Shi

и другие.

Molecular and Cellular Biochemistry, Год журнала: 2024, Номер unknown

Опубликована: Дек. 2, 2024

Язык: Английский

Процитировано

0