Fluorinated hydroxyapatite conditions a favorable osteo-immune microenvironment via triggering metabolic shift from glycolysis to oxidative phosphorylation DOI Creative Commons
Kaidi Chen, Seongmin Ha, Leyao Xu

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: May 8, 2024

Biological-derived hydroxyapatite is widely used as a bone substitute for addressing defects, but its limited osteoconductive properties necessitate further improvement. The osteo-immunomodulatory hold crucial promise in maintaining homeostasis, and precise modulation of macrophage polarization essential this process. Metabolism serves guiding force immunity, fluoride modification represents promising strategy modulating the osteoimmunological environment by regulating immunometabolism. In context, we synthesized fluorinated porcine (FPHA), has demonstrated enhanced biological osteogenic capacity. However, it remains unknown whether how FPHA affects immune microenvironment defects.

Language: Английский

Lubricating MXenzyme-based hybrid hydrogel reverses oxidative damage to alleviate osteoarthritis DOI
Zhao Zhang,

Debin Cheng,

Jingxin Pan

et al.

Chemical Engineering Journal, Journal Year: 2024, Volume and Issue: 482, P. 148815 - 148815

Published: Jan. 19, 2024

Language: Английский

Citations

12

The role of mitophagy in metabolic diseases and its exercise intervention DOI Creative Commons

Shaokai Tang,

Yuanwen Geng,

Qinqin Lin

et al.

Frontiers in Physiology, Journal Year: 2024, Volume and Issue: 15

Published: Jan. 29, 2024

Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, maintain cellular homeostasis by removing damaged mitochondria participating developing diseases. Research has confirmed exercise regulate mitophagy levels, thereby exerting protective effects This article reviews role of diseases, on mitophagy, potential mechanisms exercise-regulated intervention providing new insights for future basic clinical research interventions to prevent treat

Language: Английский

Citations

9

Mitochondrial function and reactive oxygen species production during human sperm capacitation: Unraveling key players DOI
Pilar Irigoyen, Santiago Mansilla, Laura Castro

et al.

The FASEB Journal, Journal Year: 2024, Volume and Issue: 38(4)

Published: Feb. 26, 2024

Abstract Sperm capacitation is a critical process for male fertility. It involves series of biochemical and physiological changes that occur in the female reproductive tract, rendering sperm competent successful fertilization. The precise mechanisms and, specifically, role mitochondria, remain incompletely understood. Previously, we revealed mouse mitochondrial activity (e.g., oxygen consumption, membrane potential, ATP/ADP exchange, Ca 2+ ) increases during capacitation. Herein, studied function by high‐resolution respirometry (HRR) reactive species production capacitated (CAP) non‐capacitated (NC) human spermatozoa. We found from normozoospermic donors, respiratory control ratio increased 36%, accompanied double consumption rate (OCR) presence antimycin A. Extracellular hydrogen peroxide (H 2 O detection was three times higher CAP than NC cells. To confirm H depends on superoxide () formation, evaluated aconitase (ACO2) amount, activity, metabolic flux tricarboxylic acid cycle. estimated cells produce, average individual, (59 ± 22)% more steady‐state compared to Finally, analyzed two targets oxidative stress: lipid peroxidation western blot against 4‐hydroxynonenal succinate dehydrogenase (SDH) HRR. did not observe modifications lipoperoxidation nor SDH, suggesting capacitation, increase does damage it necessary normal process.

Language: Английский

Citations

9

Role of iron in brain development, aging, and neurodegenerative diseases DOI Creative Commons
Qiqi Gao, Yiyang Zhou, Yu Chen

et al.

Annals of Medicine, Journal Year: 2025, Volume and Issue: 57(1)

Published: March 4, 2025

It is now understood that iron crosses the blood-brain barrier via a complex metabolic regulatory network and participates in diverse critical biological processes within central nervous system, including oxygen transport, energy metabolism, synthesis catabolism of myelin neurotransmitters. During brain development, distributed throughout brain, playing pivotal role key such as neuronal myelination, neurotransmitter synthesis. In physiological aging, can selectively accumulate specific regions, impacting cognitive function leading to intracellular redox imbalance, mitochondrial dysfunction, lipid peroxidation, thereby accelerating aging associated pathologies. Furthermore, accumulation may be primary contributor neurodegenerative diseases Alzheimer's Parkinson's diseases. Comprehending diseases, utilizing iron-sensitive Magnetic Resonance Imaging (MRI) technology for timely detection or prediction abnormal neurological states, implementing appropriate interventions instrumental preserving normal system function.

Language: Английский

Citations

1

A Novel Nanosafety Approach Using Cell Painting, Metabolomics, and Lipidomics Captures the Cellular and Molecular Phenotypes Induced by the Unintentionally Formed Metal-Based (Nano)Particles DOI Creative Commons
Andi Alijagić, Nikolai Scherbak, Oleksandr Kotlyar

et al.

Cells, Journal Year: 2023, Volume and Issue: 12(2), P. 281 - 281

Published: Jan. 11, 2023

Additive manufacturing (AM) or industrial 3D printing uses cutting-edge technologies and materials to produce a variety of complex products. However, the effects unintentionally emitted AM (nano)particles (AMPs) on human cells following inhalation, require further investigations. The physicochemical characterization AMPs, extracted from filter Laser Powder Bed Fusion (L-PBF) printer iron-based materials, disclosed their complexity, in terms size, shape, chemistry. Cell Painting, high-content screening (HCS) assay, was used detect subtle morphological changes elicited by AMPs at single cell resolution. profiling phenotypes, prominent concentration-dependent cytoskeleton, mitochondria, membranous structures cell. Furthermore, lipidomics confirmed that induced extensive membrane remodeling lung epithelial macrophage co-culture model. To elucidate biological mechanisms action, targeted metabolomics unveiled several inflammation-related metabolites regulating response AMP exposure. Overall, exposure led internalization, oxidative stress, cytoskeleton disruption, mitochondrial activation, remodeling, metabolic reprogramming macrophages. We propose approach integrating Painting with lipidomics, as an advanced nanosafety methodology, increasing ability capture cellular molecular phenotypes relevant (nano)particle

Language: Английский

Citations

18

Wnt5a/Ca2+ signaling regulates silica-induced ferroptosis in mouse macrophages by altering ER stress-mediated redox balance DOI
Jia Ma, Jiaqi Wang,

Chenjie Ma

et al.

Toxicology, Journal Year: 2023, Volume and Issue: 490, P. 153514 - 153514

Published: April 18, 2023

Language: Английский

Citations

18

Host mitochondria: more than an organelle in SARS-CoV-2 infection DOI Creative Commons
Shahrzad Shoraka, Amali E. Samarasinghe, Amir Ghaemi

et al.

Frontiers in Cellular and Infection Microbiology, Journal Year: 2023, Volume and Issue: 13

Published: Aug. 25, 2023

Since December 2019, the world has been facing viral pandemic called COVID-19 (Coronavirus disease 2019) caused by a new beta-coronavirus named severe acute respiratory syndrome coronavirus-2, or SARS-CoV-2. patients may present with wide range of symptoms, from asymptomatic to requiring intensive care support. The form is often marked an altered immune response and cytokine storm. Advanced age, age-related underlying diseases, including metabolic syndromes, appear contribute increased severity mortality suggesting role for mitochondria in pathogenesis. Furthermore, since system associated its damage-related molecular patterns (mtDAMPs), host mitochondrial play important during infections. Viruses have evolved modulate function survival proliferation, which turn could lead cellular stress progression. Recent studies focused on possible roles SARS-CoV-2 infection. It suggested that hijacking be key factor In this review, we discuss infections infection based past knowledge. Paying attention will help better understand pathophysiology achieve effective methods prevention, diagnosis, treatment.

Language: Английский

Citations

18

PPARs and Their Neuroprotective Effects in Parkinson’s Disease: A Novel Therapeutic Approach in α-Synucleinopathy? DOI Open Access
Isaac Pérez-Segura, Alberto Santiago-Balmaseda,

Luis Daniel Rodríguez-Hernández

et al.

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(4), P. 3264 - 3264

Published: Feb. 7, 2023

Parkinson’s disease (PD) is the most common α-synucleinopathy worldwide. The pathognomonic hallmark of PD misfolding and propagation α-synuclein (α-syn) protein, observed in post-mortem histopathology. It has been hypothesized that triggers oxidative stress, mitochondrial dysfunction, neuroinflammation, synaptic leading to neurodegeneration. To this date, there are no disease-modifying drugs generate neuroprotection against these neuropathological events especially α-synucleinopathy. Growing evidence suggests peroxisome proliferator-activated receptor (PPAR) agonists confer neuroprotective effects PD, however, whether they also an anti-α-synucleinopathy effect unknown. Here we analyze reported therapeutic PPARs, specifically gamma isoform (PPARγ), preclinical animal models clinical trials for suggest possible mechanisms acting downstream from receptors. Elucidating PPARs through mimic as closely will facilitate execution better PD.

Language: Английский

Citations

17

Organ-Specific Mitochondrial Alterations Following Ischemia–Reperfusion Injury in Post-Cardiac Arrest Syndrome: A Comprehensive Review DOI Creative Commons
Eriko Nakamura, Tomoaki Aoki, Yusuke Endo

et al.

Life, Journal Year: 2024, Volume and Issue: 14(4), P. 477 - 477

Published: April 5, 2024

Background: Mitochondrial dysfunction, which is triggered by systemic ischemia–reperfusion (IR) injury and affects various organs, a key factor in the development of post-cardiac arrest syndrome (PCAS). Current research on PCAS primarily addresses generalized mitochondrial responses, resulting knowledge gap regarding organ-specific dynamics. This review focuses responses to IR injury, particularly examining brain, heart, kidneys, highlight potential therapeutic strategies targeting dysfunction enhance outcomes post-IR injury. Methods Results: We conducted narrative recent advancements related exhibit considerable variation across different organ systems, influenced unique structures, bioenergetics, antioxidative capacities. Each demonstrates distinct behaviors that have evolved fulfill specific metabolic functional needs. For example, cerebral mitochondria display dynamic can be both protective detrimental neuronal activity function during ischemic events. Cardiac show vulnerability IR-induced oxidative stress, while renal pattern fission fusion, closely linked their susceptibility acute kidney heterogeneity requires tailored interventions. Progress medicine, especially realms genomics metabolomics, paving way for innovative combat dysfunction. Emerging techniques such as transplantation hold revolutionize management resuscitation science. Conclusions: The investigation into pivotal realm research, within context PCAS. nuanced understanding holds promise revolutionizing management, addressing dysfunctions observed critical organs affected

Language: Английский

Citations

8

The Role of Mitochondria in Mediation of Skeletal Muscle Repair DOI Creative Commons
Stephen E. Alway, Hector G. Paez, Christopher R. Pitzer

et al.

Muscles, Journal Year: 2023, Volume and Issue: 2(2), P. 119 - 163

Published: March 24, 2023

Musculoskeletal health is directly linked to independence and longevity, but disease aging impairs muscle mass health. Complete repair after a pathological or physiological injury critical for maintaining function, yet compromised disuse, in conditions such as metabolic diseases, cancer, aging. Regeneration of damaged tissue critically dependent upon achieving the optimal function satellite cells (muscle stem cells, MSCs). MSC remodeling highly its microenvironment, MSCs, which on functional capacity their mitochondria. Muscle energy demanding mitochondria provide primary source production during regeneration. However, induce mitochondrial dysfunction, limits Nevertheless, role likely extends beyond ATP could potentially important regulatory signaling MSCs from injury. The scope current research regeneration molecules exosomes, largely with goal understanding ways improve function. This review focuses skeletal myogenesis/regeneration repair. A therapeutic strategy improving number will be discussed means enhancing Highlights: (a). Mitochondrial dysfunction regeneration; (b). cell (MSC) can modulated by mitochondria; (c). Enhancing may an

Language: Английский

Citations

16