Mitochondria in health, disease, and aging

Physiological Reviews, Год журнала: 2023, Номер 103(4), С. 2349 - 2422

Опубликована: Апрель 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

Язык: Английский

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Mitochondria-targeted fluorophore: State of the art and future trends

Coordination Chemistry Reviews, Год журнала: 2024, Номер 508, С. 215772 - 215772

Опубликована: Март 13, 2024

Язык: Английский

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Comprehensive review of potential drugs with anti-pulmonary fibrosis properties

Biomedicine & Pharmacotherapy, Год журнала: 2024, Номер 173, С. 116282 - 116282

Опубликована: Фев. 23, 2024

Pulmonary fibrosis is a chronic and progressive lung disease characterized by the accumulation of scar tissue in lungs, which leads to impaired function reduced quality life. The prognosis for idiopathic pulmonary (IPF), most common form fibrosis, generally poor. median survival patients with IPF estimated be around 3–5 years from time diagnosis. Currently, there are two approved drugs (Pirfenidone Nintedanib) treatment IPF. However, Pirfenidone Nintedanib not able reverse or cure fibrosis. There need new pharmacological interventions that can slow halt progression This review aims provide an updated overview current future drug summarize possible targets potential anti-pulmonary drugs, providing theoretical support further clinical combination therapy development drugs.

Язык: Английский

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Elevating VAPB-PTPIP51 integration repairs damaged mitochondria-associated endoplasmic reticulum membranes and inhibits lung fibroblasts activation

International Immunopharmacology, Год журнала: 2025, Номер 147, С. 113982 - 113982

Опубликована: Янв. 5, 2025

Язык: Английский

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Mitochondrial Transfer from Mesenchymal Stem Cells to Macrophages Restricts Inflammation and Alleviates Kidney Injury in Diabetic Nephropathy Mice via PGC-1α Activation

Stem Cells, Год журнала: 2021, Номер 39(7), С. 913 - 928

Опубликована: Апрель 16, 2021

Abstract Mesenchymal stem cells (MSCs) have fueled ample translation for treatment of immune-mediated diseases. Our previous study had demonstrated that MSCs could elicit macrophages (Mφ) into anti-inflammatory phenotypes, and alleviate kidney injury in diabetic nephropathy (DN) mice via improving mitochondrial function Mφ, yet the specific mechanism was unclear. Recent evidence indicated communicated with their microenvironment through exchanges mitochondria. By a coculture system consisting we showed MSCs-derived mitochondria (MSCs-Mito) were transferred functions improved, which contributed to M2 polarization. Furthermore, found MSCs-Mito transfer activated peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α)-mediated biogenesis. In addition, PGC-1α interacted TFEB high glucose-induced leading elevated lysosome-autophagy, essential removal damaged As result, bioenergy capacity combat inflammatory response enhanced. Whereas, immune-regulatory activity significantly blocked knockdown Mφ. More importantly, be observed DN mice, adoptive educated Mφ (MφMito) inhibited alleviated injury. However, kidney-protective effects MφMito abolished when impaired rotenone, similar results also transfected sipgc-1α before administration. Collectively, these findings suggested elicited phenotype ameliorated relied on PGC-1α-mediated biogenesis PGC-1α/TFEB-mediated lysosome-autophagy.

Язык: Английский

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Nanotherapies for sepsis by regulating inflammatory signals and reactive oxygen and nitrogen species: New insight for treating COVID-19

Redox Biology, Год журнала: 2021, Номер 45, С. 102046 - 102046

Опубликована: Июнь 15, 2021

SARS-CoV-2 has caused up to 127 million cases of COVID-19. Approximately 5% COVID-19 patients develop severe illness, and approximately 40% those with illness eventually die, corresponding more than 2.78 people. The pathological characteristics resemble typical sepsis, been identified as viral sepsis. Progress in sepsis research is important for improving the clinical care these patients. Recent advances understanding pathogenesis have led view that an uncontrolled inflammatory response oxidative stress are core factors. However, traditional treatment it difficult achieve a balance between inflammation, pathogens (viruses, bacteria, fungi), patient tolerance, resulting high mortality In recent years, nanomaterials mediating reactive oxygen nitrogen species (RONS) shown previously unattainable therapeutic effects on Despite advantages, RONS response-based yet be extensively adopted therapy. To best our knowledge, no review discussed application nanomaterials. help bridge this gap, we discuss related inflammation overproduction RONS, which activate pathogen-associated molecular pattern (PAMP)-pattern recognition receptor (PRR) damage-associated (DAMP)-PRR signaling pathways. We also summarize As highlighted here, strategy could synergistically improve efficacy against both may prolong survival. Current challenges future developments summarized.

Язык: Английский

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Inhibition of lung microbiota-derived proapoptotic peptides ameliorates acute exacerbation of pulmonary fibrosis

Nature Communications, Год журнала: 2022, Номер 13(1)

Опубликована: Март 23, 2022

Abstract Idiopathic pulmonary fibrosis is an incurable disease of unknown etiology. Acute exacerbation idiopathic associated with high mortality. Excessive apoptosis lung epithelial cells occurs in acute exacerbation. We recently identified corisin, a proapoptotic peptide that triggers fibrosis. Here, we provide insights into the mechanism underlying processing and release corisin. Furthermore, demonstrate anticorisin monoclonal antibody ameliorates by significantly inhibiting human transforming growth factorβ1 model injury bleomycin model. By investigating impact general injury, further unravel potential corisin to such diseases. These results underscore role pathogenesis novel approach treating this disease.

Язык: Английский

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CD38 Mediates Lung Fibrosis by Promoting Alveolar Epithelial Cell Aging

American Journal of Respiratory and Critical Care Medicine, Год журнала: 2022, Номер 206(4), С. 459 - 475

Опубликована: Июнь 6, 2022

A prevailing paradigm recognizes idiopathic pulmonary fibrosis (IPF) originating from various alveolar epithelial cell (AEC) injuries, and there is a growing appreciation of AEC aging as key driver the pathogenesis. Despite this progress, it incompletely understood what main factor(s) contribute to worsened in lung fibrosis. It remains challenge how dampen thereby mitigate disease progression.

Язык: Английский

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Connective Tissue Growth Factor in Idiopathic Pulmonary Fibrosis: Breaking the Bridge

International Journal of Molecular Sciences, Год журнала: 2022, Номер 23(11), С. 6064 - 6064

Опубликована: Май 28, 2022

CTGF is upregulated in patients with idiopathic pulmonary fibrosis (IPF), characterized by the deposition of a pathological extracellular matrix (ECM). Additionally, many omics studies confirmed that aberrant cellular senescence-associated mitochondria dysfunction and metabolic reprogramming had been identified different IPF lung cells (alveolar epithelial cells, alveolar endothelial fibroblasts, macrophages). Here, we reviewed role to mediate anomalous senescence-related mechanisms support fibrotic environment IPF.

Язык: Английский

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microRNA-33 deficiency in macrophages enhances autophagy, improves mitochondrial homeostasis, and protects against lung fibrosis

JCI Insight, Год журнала: 2023, Номер 8(4)

Опубликована: Янв. 10, 2023

Idiopathic pulmonary fibrosis (IPF) is a progressive and ultimately fatal disease. Recent findings have shown marked metabolic reprogramming associated with changes in mitochondrial homeostasis autophagy during fibrosis. The microRNA-33 (miR-33) family of microRNAs (miRNAs) encoded within the introns sterol regulatory element binding protein (SREBP) genes are master regulators fatty acid (FA) metabolism. miR-33 controls macrophage immunometabolic response enhances biogenesis, FA oxidation, cholesterol efflux. Here, we show that levels increased bronchoalveolar lavage (BAL) cells isolated from patients IPF compared healthy controls. We demonstrate specific genetic ablation macrophages protects against bleomycin-induced absence improves increases while decreasing inflammatory after bleomycin injury. Notably, pharmacological inhibition via administration anti-miR-33 peptide nucleic acids (PNA-33) attenuates different vivo ex mice human models These studies elucidate major role regulation uncover potentially novel therapeutic approach to treat this

Язык: Английский

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