Mitochondrial Glucocorticoid Receptors and Their Actions DOI Open Access
Ioanna Kokkinopoulou, Paraskevi Moutsatsou

International Journal of Molecular Sciences, Journal Year: 2021, Volume and Issue: 22(11), P. 6054 - 6054

Published: June 3, 2021

Mitochondria are membrane organelles present in almost all eukaryotic cells. In addition to their well-known role energy production, mitochondria regulate central cellular processes, including calcium homeostasis, Reactive Oxygen Species (ROS) generation, cell death, thermogenesis, and biosynthesis of lipids, nucleic acids, steroid hormones. Glucocorticoids (GCs) the mitochondrially encoded oxidative phosphorylation gene expression mitochondrial metabolism. The identification Glucocorticoid Response Elements (GREs) sequences detection Receptor (GR) different types gave support hypothesis that GR directly regulates expression. Numerous studies have revealed changes alongside with import/export mitochondria, confirming direct effects GCs on genome. Further evidence has made clear is involved function apoptosis-mediated through interacting or altering distribution Bcl2 family members. Even though its exact translocation mechanisms remain unknown, data shown chaperones (Hsp70/90, Bag-1, FKBP51), anti-apoptotic protein Bcl-2, HDAC6- mediated deacetylation outer complexes (Tom complexes) co-ordinate trafficking. A stress depression as well lung hepatic inflammation also been demonstrated.

Language: Английский

Phase Separation and Neurodegenerative Diseases: A Disturbance in the Force DOI Creative Commons
Aurélie Zbinden, Manuela Pérez‐Berlanga, Pierre De Rossi

et al.

Developmental Cell, Journal Year: 2020, Volume and Issue: 55(1), P. 45 - 68

Published: Oct. 1, 2020

Language: Английский

Citations

382
Mitochondria in health, disease, and aging DOI
John S. Harrington, Stefan W. Ryter, Maria Plataki

et al.

Physiological Reviews, Journal Year: 2023, Volume and Issue: 103(4), P. 2349 - 2422

Published: April 6, 2023

Mitochondria are well known as organelles responsible for the maintenance of cellular bioenergetics through production ATP. Although oxidative phosphorylation may be their most important function, mitochondria also integral synthesis metabolic precursors, calcium regulation, reactive oxygen species, immune signaling, and apoptosis. Considering breadth responsibilities, fundamental metabolism homeostasis. Appreciating this significance, translational medicine has begun to investigate how mitochondrial dysfunction can represent a harbinger disease. In review, we provide detailed overview metabolism, bioenergetics, dynamics, autophagy, damage-associated molecular patterns, mitochondria-mediated cell death pathways, at any these levels is associated with disease pathogenesis. Mitochondria-dependent pathways thereby an attractive therapeutic target ameliorating human

Language: Английский

Citations

286
Mitochondrial Dysfunction, Oxidative Stress, and Neuroinflammation: Intertwined Roads to Neurodegeneration DOI Creative Commons
Anna Picca, Riccardo Calvani, Hélio José Coelho‐Júnior

et al.

Antioxidants, Journal Year: 2020, Volume and Issue: 9(8), P. 647 - 647

Published: July 22, 2020

Oxidative stress develops as a response to injury and reflects breach in the cell’s antioxidant capacity. Therefore, fine-tuning of reactive oxygen species (ROS) generation is crucial for preserving homeostasis. Mitochondria are major source an immediate target ROS. Under different stimuli, including oxidative impaired quality control, mitochondrial constituents (e.g., DNA, mtDNA) displaced toward intra- or extracellular compartments. However, mechanisms responsible mtDNA unloading remain largely unclear. While shuttling freely within cell, can be delivered into compartment via either extrusion entire nucleoids release vesicles. Once discarded, may act damage-associated molecular pattern (DAMP) trigger innate immune inflammatory by binding danger-signal receptors. Neuroinflammation associated with large array neurological disorders which DAMPs could represent common thread supporting disease progression. The exploration non-canonical pathways involved control neurodegeneration unveil novel targets development therapeutic agents. Here, we discuss these processes setting two neurodegenerative diseases (Alzheimer’s Parkinson’s disease) Down syndrome, most frequent progeroid syndrome.

Language: Английский

Citations

267
Defective mitophagy in Alzheimer’s disease DOI
Jangampalli Adi Pradeepkiran, P. Hemachandra Reddy

Ageing Research Reviews, Journal Year: 2020, Volume and Issue: 64, P. 101191 - 101191

Published: Oct. 3, 2020

Language: Английский

Citations

261
Regulation of Mitochondrial ATP Production: Ca2+ Signaling and Quality Control DOI
Liron Boyman, Mariusz Karbowski, W. Jonathan Lederer

et al.

Trends in Molecular Medicine, Journal Year: 2019, Volume and Issue: 26(1), P. 21 - 39

Published: Nov. 22, 2019

Language: Английский

Citations

218
Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism DOI Creative Commons
Zhifu Cui, Xingtao Zhao, Felix Kwame Amevor

et al.

Frontiers in Immunology, Journal Year: 2022, Volume and Issue: 13

Published: July 22, 2022

Quercetin, a naturally non-toxic flavonoid within the safe dose range with antioxidant, anti-apoptotic and anti-inflammatory properties, plays an important role in treatment of aging-related diseases. Sirtuin 1 (SIRT1), member NAD+-dependent deacetylase enzyme family, is extensively explored as potential therapeutic target for attenuating aging-induced disorders. SIRT1 possess beneficial effects against diseases such Alzheimer's disease (AD), Parkinson's (PD), Huntington's (HD), Depression, Osteoporosis, Myocardial ischemia (M/I) reperfusion (MI/R), Atherosclerosis (AS), Diabetes. Previous studies have reported that aging increases tissue susceptibility, whereas, regulates cellular senescence multiple processes, including SIRT1/Keap1/Nrf2/HO-1 SIRTI/PI3K/Akt/GSK-3β mediated oxidative stress, SIRT1/NF-κB SIRT1/NLRP3 regulated inflammatory response, SIRT1/PGC1α/eIF2α/ATF4/CHOP SIRT1/PKD1/CREB controlled phosphorylation, SIRT1-PINK1-Parkin mitochondrial damage, SIRT1/FoxO autophagy, SIRT1/FoxG1/CREB/BDNF/Trkβ-catenin neuroprotective effects. In this review, we summarized improvement attenuation effect quercetin on relationship between relevant signaling pathways by SIRT1. Moreover, functional regulation markers function, autophagy apoptosis through was discussed. Finally, prospects extracellular vesicles (EVs) loading delivery, SIRT1-mediated EVs signal carriers treating diseases, well discussed ferroptosis alleviation to protect via activating Generally, may serve promising inhibiting reducing responses, restoring dysfunction.

Language: Английский

Citations

210
PPARγ/PGC1α signaling as a potential therapeutic target for mitochondrial biogenesis in neurodegenerative disorders DOI
Sumit Jamwal, Jennifer K. Blackburn, John D. Elsworth

et al.

Pharmacology & Therapeutics, Journal Year: 2020, Volume and Issue: 219, P. 107705 - 107705

Published: Oct. 9, 2020

Language: Английский

Citations

143
The Role of Taurine in Mitochondria Health: More Than Just an Antioxidant DOI Creative Commons
Chian Ju Jong,

Priyanka Sandal,

Stephen W. Schaffer

et al.

Molecules, Journal Year: 2021, Volume and Issue: 26(16), P. 4913 - 4913

Published: Aug. 13, 2021

Taurine is a naturally occurring sulfur-containing amino acid that found abundantly in excitatory tissues, such as the heart, brain, retina and skeletal muscles. was first isolated 1800s, but not much known about this molecule until 1990s. In 1985, taurine approved treatment among heart failure patients Japan. Accumulating studies have shown supplementation also protects against pathologies associated with mitochondrial defects, aging, diseases, metabolic syndrome, cancer, cardiovascular diseases neurological disorders. review, we will provide general overview on mitochondria biology consequence of defects pathologies. Then, discuss antioxidant action taurine, particularly relation to maintenance function. We describe several reported current use mitochondria-associated humans.

Language: Английский

Citations

140
The neuroprotective effects of glucagon-like peptide 1 in Alzheimer’s and Parkinson’s disease: An in-depth review DOI Creative Commons
Niklas Reich, Christian Hölscher

Frontiers in Neuroscience, Journal Year: 2022, Volume and Issue: 16

Published: Sept. 1, 2022

Currently, there is no disease-modifying treatment available for Alzheimer's and Parkinson's disease (AD PD) that includes the highly controversial approval of Aβ-targeting antibody aducanumab AD. Hence, still an unmet need a neuroprotective drug in both AD PD. Type 2 diabetes risk factor Glucagon-like peptide 1 (GLP-1) hormone growth has shown effects preclinical studies, success GLP-1 mimetics phase II clinical trials PD raised new hope. are currently on market as treatments type diabetes. analogs safe, well tolerated, resistant to desensitization characterized clinic. Herein, we review existing evidence illustrate pathways induced following GLP-1R activation neurons, microglia astrocytes. The latter include synaptic protection, improvements cognition, learning motor function, amyloid pathology-ameliorating properties (Aβ, Tau, α-synuclein), suppression Ca

Language: Английский

Citations

116
Aging, oxidative stress and degenerative diseases: mechanisms, complications and emerging therapeutic strategies DOI
Mani Raj Chaudhary, Sakshi Chaudhary, Yogita Sharma

et al.

Biogerontology, Journal Year: 2023, Volume and Issue: 24(5), P. 609 - 662

Published: July 30, 2023

Language: Английский

Citations

80