Calcium bridges built by mitochondria-associated endoplasmic reticulum membranes: potential targets for neural repair in neurological diseases DOI Creative Commons

Yichen Peng,

Li Zhou,

Yaju Jin

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(12), P. 3349 - 3369

Published: Nov. 13, 2024

The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions metabolic levels. Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels the membrane mitochondrial outer membrane, formed by various proteins protein complexes. This microstructural domain mediates several specialized functions, including calcium (Ca 2+ ) signaling, autophagy, morphology, oxidative stress response, apoptosis. Notably, dysregulation Ca signaling mediated mitochondria-associated is critical factor pathogenesis neurological diseases. Certain or complexes within these directly indirectly regulate distance mitochondria, well transduction signaling. Conversely, influences other membrane-associated functions. These can vary significantly across different diseases—such ischemic stroke, traumatic brain injury, Alzheimer’s disease, Parkinson’s amyotrophic lateral sclerosis, Huntington’s disease—and their respective stages progression. Targeted modulation disease-related pathways functional enhance function promote regeneration repair damaged neurons. Therefore, membranes-mediated pivotal pathological progression diseases represents significant potential therapeutic target. review focuses on effects distinct roles diseases, specifically highlighting early protective neuronal damage that result from prolonged overload deficiency. article provides comprehensive analysis mechanisms contributing to exploration targets for promoting neuroprotection nerve repair.

Language: Английский

Intranasal Insulin Administration Affecting Perioperative Neurocognitive Dysfunction by Regulating Calcium Transport Protein Complex IP3R/GRP75/VDAC1 on MAMs DOI
Huiqin Liu, Yanhua Jiang, Cong Lin

et al.

Free Radical Biology and Medicine, Journal Year: 2025, Volume and Issue: 228, P. 240 - 250

Published: Jan. 5, 2025

Language: Английский

Citations

0
Zn2+ protects H9C2 cardiomyocytes by alleviating MAMs-associated apoptosis and calcium signaling dysregulation DOI

Jiabao Guo,

Tingting Ma,

Bingyu Wang

et al.

Cellular Signalling, Journal Year: 2025, Volume and Issue: unknown, P. 111629 - 111629

Published: Jan. 1, 2025

Language: Английский

Citations

0
Endoplasmic reticulum stress signaling modulates ischemia/reperfusion injury in the aged heart by regulating mitochondrial maintenance DOI Creative Commons
Ji Zhang, Yuanyuan Zhao, Nianqiao Gong

et al.

Molecular Medicine, Journal Year: 2024, Volume and Issue: 30(1)

Published: July 23, 2024

Abstract Aging is associated with an increased risk of myocardial ischemia/reperfusion injury (IRI). With increasing prevalence cardiovascular diseases such as coronary arteriosclerosis in older people, there has been interest understanding the mechanisms IRI to develop therapeutics that can attenuate its damaging effects. Previous studies identified abnormal mitochondria, involved cellar senescence and oxidative stress, are master subcellular organelle induces IRI. In addition, endoplasmic reticulum (ER) stress also Cellular adaptation ER achieved by activation molecular chaperones folding enzymes, which provide important link between gene programs. this review, we outline how these stress-related molecules affect via crosstalk mitochondrial homeostasis discuss may offer promising novel therapeutic targets strategies against age-related diseases.

Language: Английский

Citations

2
Reduction of Mitochondrial Calcium Overload via MKT077-Induced Inhibition of Glucose-Regulated Protein 75 Alleviates Skeletal Muscle Pathology in Dystrophin-Deficient mdx Mice DOI Open Access
Mikhail V. Dubinin, Anastasia E. Stepanova, I. B. Mikheeva

et al.

International Journal of Molecular Sciences, Journal Year: 2024, Volume and Issue: 25(18), P. 9892 - 9892

Published: Sept. 13, 2024

Duchenne muscular dystrophy is secondarily accompanied by Ca2+ excess in muscle fibers. Part of the accumulates mitochondria, contributing to development mitochondrial dysfunction and degeneration muscles. In this work, we assessed effect intraperitoneal administration rhodacyanine MKT077 (5 mg/kg/day), which able suppress glucose-regulated protein 75 (GRP75)-mediated transfer from sarcoplasmic reticulum (SR) on overload skeletal mitochondria dystrophin-deficient mdx mice concomitant pathology. prevented quadriceps mice, reduced intensity oxidative stress, improved ultrastructure, but had no impaired phosphorylation. eliminated calcification fiber degeneration, fibrosis level, normalized grip strength mice. However, noted a negative wild-type expressed as decrease efficiency phosphorylation, SR stress development, ultrastructural disturbances quadriceps, reduction animal endurance wire-hanging test. This paper discusses impact modulation pathology

Language: Английский

Citations

2
Emerging and Novel Therapeutic Treatments Targeting Mitochondrial-Endoplasmic Reticulum Contact Sites in Metabolic and Vascular Disorders DOI
Richard M. Monaghan

International Journal of Drug Discovery and Pharmacology, Journal Year: 2024, Volume and Issue: unknown, P. 100008 - 100008

Published: June 6, 2024

Review Emerging and Novel Therapeutic Treatments Targeting Mitochondrial-Endoplasmic Reticulum Contact Sites in Metabolic Vascular Disorders Richard M. Monaghan The British Heart Foundation Centre of Research Excellence Manchester, Division Cardiovascular Sciences, Faculty Biology, Medicine, Health, University AV Hill Building, Oxford Road, M13 9PN, UK;[email protected] Received: 10 April 2024; Revised: 5 May Accepted: 7 Published: 6 June 2024 Abstract: Subcellular organellar contact sites, particularly those between mitochondria the endoplasmic reticulum (MERCSs), play crucial roles maintaining health. These specialized partitions facilitate vital communication organelles, regulating processes essential for cell function, including calcium balance, lipid biogenesis transport, mitochondrial dynamics, programmed death. Growing evidence shows that perturbation MERCSs contributes significantly to various diseases, neurodegenerative disorders like Alzheimer’s Parkinson’s, metabolic issues, such as type 2 diabetes, heart conditions, cancer. This review dives into this expanding field, exploring potential therapeutic targets. It provides a detailed overview proteins form maintain MERCSs, highlighting how their disruption can lead cellular dysfunction disease. Additionally, it examines recent exciting breakthroughs developing drugs strategies manipulate clinical benefits. While challenges remain, emphasises MERCS-based therapies outlines critical research needed move these treatments from lab clinic.

Language: Английский

Citations

1
Calcium bridges built by mitochondria-associated endoplasmic reticulum membranes: potential targets for neural repair in neurological diseases DOI Creative Commons

Yichen Peng,

Li Zhou,

Yaju Jin

et al.

Neural Regeneration Research, Journal Year: 2024, Volume and Issue: 20(12), P. 3349 - 3369

Published: Nov. 13, 2024

The exchange of information and materials between organelles plays a crucial role in regulating cellular physiological functions metabolic levels. Mitochondria-associated endoplasmic reticulum membranes serve as physical contact channels the membrane mitochondrial outer membrane, formed by various proteins protein complexes. This microstructural domain mediates several specialized functions, including calcium (Ca 2+ ) signaling, autophagy, morphology, oxidative stress response, apoptosis. Notably, dysregulation Ca signaling mediated mitochondria-associated is critical factor pathogenesis neurological diseases. Certain or complexes within these directly indirectly regulate distance mitochondria, well transduction signaling. Conversely, influences other membrane-associated functions. These can vary significantly across different diseases—such ischemic stroke, traumatic brain injury, Alzheimer’s disease, Parkinson’s amyotrophic lateral sclerosis, Huntington’s disease—and their respective stages progression. Targeted modulation disease-related pathways functional enhance function promote regeneration repair damaged neurons. Therefore, membranes-mediated pivotal pathological progression diseases represents significant potential therapeutic target. review focuses on effects distinct roles diseases, specifically highlighting early protective neuronal damage that result from prolonged overload deficiency. article provides comprehensive analysis mechanisms contributing to exploration targets for promoting neuroprotection nerve repair.

Language: Английский

Citations

0