Mitochondria transfer for myelin repair DOI Creative Commons
Sabah Mozafari, Luca Peruzzotti‐Jametti, Stefano Pluchino

et al.

Journal of Cerebral Blood Flow & Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: March 13, 2025

Demyelination is a common feature of neuroinflammatory and degenerative diseases the central nervous system (CNS), such as multiple sclerosis (MS). It often linked to disruptions in intercellular communication, bioenergetics metabolic balance accompanied by mitochondrial dysfunction cells oligodendrocytes, neurons, astrocytes, microglia. Although current MS treatments focus on immunomodulation, they fail stop or reverse demyelination’s progression. Recent advancements highlight exchange promising therapeutic target, with potential restore homeostasis, enhance promote myelin repair. With this review we will provide insights into CNS decoupling, focusing role demyelinating conditions. We then discuss emerging cell-free biotherapies exploring transferring mitochondria via biogenic carriers like extracellular vesicles (EVs) synthetic liposomes, aimed at enhancing function support for Lastly, address key challenges clinical application these strategies future directions optimize biotherapies. The field hold promise restoring repair, potentially transforming landscape diseases.

Language: Английский

Mitochondria at the crossroads of health and disease DOI Creative Commons
Anu Suomalainen, Jodi Nunnari

Cell, Journal Year: 2024, Volume and Issue: 187(11), P. 2601 - 2627

Published: May 1, 2024

Mitochondria reside at the crossroads of catabolic and anabolic metabolism—the essence life. How their structure function are dynamically tuned in response to tissue-specific needs for energy, growth repair, renewal is being increasingly understood. respond intrinsic extrinsic stresses can alter cell organismal by inducing metabolic signaling within cells distal tissues. Here, we review how centrality mitochondrial functions manifests health a broad spectrum diseases aging.

Language: Английский

Citations

105

Molecular mechanisms of mitochondrial dynamics DOI
Luis Carlos Tábara, Mayuko Segawa, Julien Prudent

et al.

Nature Reviews Molecular Cell Biology, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 17, 2024

Language: Английский

Citations

30

Targeting mitophagy in neurodegenerative diseases DOI
Odetta Antico, Paul Thompson, Nicholas T. Hertz

et al.

Nature Reviews Drug Discovery, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 14, 2025

Language: Английский

Citations

11

Recommendations for mitochondria transfer and transplantation nomenclature and characterization DOI Creative Commons
Jonathan R. Brestoff, Keshav K. Singh, Katia Aquilano

et al.

Nature Metabolism, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 16, 2025

Language: Английский

Citations

4

Extracellular Mitochondrial‐Derived Vesicles Affect the Progression of Diabetic Foot Ulcer by Regulating Oxidative Stress and Mitochondrial Dysfunction DOI Creative Commons
Huihui Zhang,

Zi Yan,

Junyou Zhu

et al.

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 21, 2025

Diabetic foot ulcer (DFU) is a common and severe complication of diabetes mellitus, the etiology which remains insufficiently understood, particularly regarding involvement extracellular vesicles (EVs). In this study, nanoflow cytometry to detect EVs in DFU skin tissues used found significant increase Translocase Outer Mitochondrial Membrane 20 (TOM20)+ mitochondrial-derived (MDVs). The role MDVs yet be reported. Using single-cell datasets, it discovered that may regulated by Sorting Nexin 9 (SNX9). vitro experiments revealed secreted fibroblasts cultured high glucose medium exhibited similar composition protein enrichment results those tissues, suggesting their potential as an ideal surrogate. These promoted apoptosis intracellular oxidative stress, disrupted mitochondrial structure, reduced aerobic metabolism target cells. vivo also showed MDV drops hindered wound healing diabetic mice; however, effect rescued SNX9 inhibitors, restoring dynamics balance. Under conditions, significantly upregulated stress levels induced dysfunction. This study proposes targeting therapeutic strategy for DFU.

Language: Английский

Citations

4

Mitochondrial protein import stress DOI
Nikolaus Pfanner, Fabian den Brave, Thomas Becker

et al.

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

Published: Jan. 22, 2025

Language: Английский

Citations

3

Compositionally unique mitochondria in filopodia support cellular migration DOI
Madeleine Marlar-Pavey, Daniel Tapias-Gomez, Marcel Mettlen

et al.

Current Biology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 1, 2025

Language: Английский

Citations

2

ATAD1 prevents clogging of TOM and damage caused by un-imported mitochondrial proteins DOI Creative Commons
J. Kim, Madeleine Goldstein,

Lauren Zecchel

et al.

Cell Reports, Journal Year: 2024, Volume and Issue: 43(8), P. 114473 - 114473

Published: July 17, 2024

Language: Английский

Citations

16

Mitochondrial derived vesicles‐ Quo Vadis? DOI Creative Commons
Ronen Hazan, Ophry Pines, Ann Saada

et al.

FEBS Journal, Journal Year: 2024, Volume and Issue: 291(21), P. 4660 - 4669

Published: Feb. 27, 2024

Mitochondria are dynamic, intracellular organelles with a separate genome originating from prokaryotes. They perform numerous functions essential for cellular metabolism and energy production. Mitochondrial‐derived vesicles (MDVs) single or double membrane‐enclosed vesicles, formed released the mitochondrial sub‐compartments into cytosol, in response to various triggers. MDVs interact other such as lysosomes peroxisomes may be incorporated excreted via extracellular (EVs). selectively incorporate diverse protein lipid cargoes involved quality control, immunomodulation, complementation, compartmentalization transport. This review aims provide summary of current knowledge biogenesis, release, cargoes, roles.

Language: Английский

Citations

10

Targeting organ-specific mitochondrial dysfunction to improve biological aging DOI Creative Commons
Corina T. Madreiter‐Sokolowski, Ursula Hiden, Jelena Krstić

et al.

Pharmacology & Therapeutics, Journal Year: 2024, Volume and Issue: 262, P. 108710 - 108710

Published: Aug. 22, 2024

In an aging society, unveiling new anti-aging strategies to prevent and combat aging-related diseases is of utmost importance. Mitochondria are the primary ATP production sites key regulators programmed cell death. Consequently, these highly dynamic organelles play a central role in maintaining tissue function, mitochondrial dysfunction pivotal factor progressive age-related decline cellular homeostasis organ function. The current review examines recent advances understanding interplay between organ-specific aging. Thereby, we dissect molecular mechanisms underlying impairment associated with deterioration exploring DNA, reactive oxygen species homeostasis, metabolic activity, damage-associated patterns, biogenesis, turnover, dynamics. We also highlight emerging therapeutic preclinical clinical tests that supposed rejuvenate such as antioxidants, biogenesis stimulators, modulators turnover Furthermore, discuss potential benefits challenges use interventions, emphasizing need for approaches given unique characteristics different tissues. conclusion, this highlights addressing mitigate aging, focusing on skin, liver, lung, brain, skeletal muscle, well reproductive, immune, cardiovascular systems. Based comprehensive multifaceted roles mitochondria, innovative may be developed optimized biological promote healthy across diverse

Language: Английский

Citations

10