Harnessing Natural Saponins: Advancements in Mitochondrial Dysfunction and Therapeutic Applications DOI

Hongmei Liu,

Huan Wang, Xinyu Lin

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: 138, P. 156383 - 156383

Published: Jan. 10, 2025

Language: Английский

A break in mitochondrial endosymbiosis as a basis for inflammatory diseases DOI
Michael P. Murphy, Luke O'neill

Nature, Journal Year: 2024, Volume and Issue: 626(7998), P. 271 - 279

Published: Feb. 7, 2024

Language: Английский

Citations

55

Diverse functions of cytochrome c in cell death and disease DOI
Zhuan Zhou, Tasnim Arroum, Xu Luo

et al.

Cell Death and Differentiation, Journal Year: 2024, Volume and Issue: 31(4), P. 387 - 404

Published: March 23, 2024

Language: Английский

Citations

55

TFAM is an autophagy receptor that limits inflammation by binding to cytoplasmic mitochondrial DNA DOI
Hao Liu,

Cien Zhen,

Jianming Xie

et al.

Nature Cell Biology, Journal Year: 2024, Volume and Issue: 26(6), P. 878 - 891

Published: May 23, 2024

Language: Английский

Citations

37

In situ architecture of Opa1-dependent mitochondrial cristae remodeling DOI Creative Commons
Michelle Y. Fry, Paula P. Navarro, Pusparanee Hakim

et al.

The EMBO Journal, Journal Year: 2024, Volume and Issue: 43(3), P. 391 - 413

Published: Jan. 15, 2024

Abstract Cristae membrane state plays a central role in regulating mitochondrial function and cellular metabolism. The protein Optic atrophy 1 (Opa1) is an important crista remodeler that exists as two forms the mitochondrion, membrane-anchored long form (l-Opa1) processed short (s-Opa1). mechanisms for how Opa1 influences cristae shape have remained unclear due to lack of native three-dimensional views cristae. We perform situ cryo-electron tomography cryo-focused ion beam milled mouse embryonic fibroblasts with defined states understand each architecture. In our tomograms, we observe variety shapes distinct trends dependent on s-Opa1:l-Opa1 balance. Increased l-Opa1 levels promote stacking elongated mitochondria, while increased s-Opa1 correlated irregular packing round mitochondria shape. Functional assays indicate wild-type apoptotic calcium handling responses, show compromised respiratory under imbalance. summary, provide visualization architecture reveal relationships between ultrastructure Opa1-mediated remodeling.

Language: Английский

Citations

23

Mitochondrial dysfunction in sepsis: mechanisms and therapeutic perspectives DOI Creative Commons
Dongxue Hu,

Harshini Sheeja Prabhakaran,

Liang Yu

et al.

Critical Care, Journal Year: 2024, Volume and Issue: 28(1)

Published: Sept. 3, 2024

Sepsis is a severe medical condition characterized by systemic inflammatory response, often culminating in multiple organ dysfunction and high mortality rates. In recent years, there has been growing recognition of the pivotal role played mitochondrial damage driving progression sepsis. Various factors contribute to impairment during sepsis, encompassing mechanisms such as reactive nitrogen/oxygen species generation, mitophagy inhibition, dynamics change, membrane permeabilization. Damaged mitochondria actively participate shaping milieu triggering key signaling pathways, including those mediated Toll-like receptors, NOD-like cyclic GMP-AMP synthase. Consequently, surge interest developing therapeutic strategies targeting mitigate septic pathogenesis. This review aims delve into intricate underpinning sepsis its significant impact on immune dysregulation. Moreover, we spotlight promising mitochondria-targeted interventions that have demonstrated efficacy preclinical models.

Language: Английский

Citations

19

The roles of mitochondria in global and local intracellular calcium signalling DOI
Benjamín Cartes-Saavedra, Arijita Ghosh, György Hajnóczky

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 27, 2025

Language: Английский

Citations

5

Targeting Mitochondrial Dysfunction in Cerebral Ischemia: Advances in Pharmacological Interventions DOI Creative Commons
И. Ф. Беленичев, Olena Popazova, Nina Bukhtiyarova

et al.

Antioxidants, Journal Year: 2025, Volume and Issue: 14(1), P. 108 - 108

Published: Jan. 18, 2025

The study of mitochondrial dysfunction has become increasingly pivotal in elucidating the pathophysiology various cerebral pathologies, particularly neurodegenerative disorders. Mitochondria are essential for cellular energy metabolism, regulation reactive oxygen species (ROS), calcium homeostasis, and execution apoptotic processes. Disruptions function, driven by factors such as oxidative stress, excitotoxicity, altered ion balance, lead to neuronal death contribute cognitive impairments several brain diseases. Mitochondrial can arise from genetic mutations, ischemic events, hypoxia, other environmental factors. This article highlights critical role progression diseases discusses need targeted therapeutic strategies attenuate damage, restore enhance neuroprotection.

Language: Английский

Citations

3

Mitochondria: An overview of their origin, genome, architecture, and dynamics DOI

João P Moura,

Paulo J. Oliveira, Ana M. Urbano

et al.

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Journal Year: 2025, Volume and Issue: unknown, P. 167803 - 167803

Published: March 1, 2025

Language: Английский

Citations

3

Apoptosis and eryptosis: similarities and differences DOI
Anton Tkachenko

APOPTOSIS, Journal Year: 2023, Volume and Issue: 29(3-4), P. 482 - 502

Published: Nov. 30, 2023

Language: Английский

Citations

33

Mechanisms of action of the BCL-2 inhibitor venetoclax in multiple myeloma: a literature review DOI Creative Commons
Qiang Cao, Xinyan Wu, Qi Zhang

et al.

Frontiers in Pharmacology, Journal Year: 2023, Volume and Issue: 14

Published: Nov. 6, 2023

Abnormal cellular apoptosis plays a pivotal role in the pathogenesis of Multiple Myeloma (MM). Over years, BCL-2, crucial anti-apoptotic protein, has garnered significant attention MM therapeutic research. Venetoclax (VTC), small-molecule targeted agent, effectively inhibits promoting programmed death cancerous cells. While VTC been employed to treat various hematological malignancies, its particular efficacy showcased potential for broader clinical applications. In this review, we delve into intricacies how modulates cells by targeting BCL-2 and overarching influence protein family regulation. Our findings highlight nuanced interplay between VTC, MM, offering insights that may pave way optimizing strategies. Through comprehensive analysis, aim lay solid groundwork future explorations VTC’s applications profound effects on apoptosis.

Language: Английский

Citations

30