Defining roles of specific reactive oxygen species (ROS) in cell biology and physiology

Nature Reviews Molecular Cell Biology, Journal Year: 2022, Volume and Issue: 23(7), P. 499 - 515

Published: Feb. 21, 2022

Language: Английский

---

Oxidative stress and regeneration

Free Radical Biology and Medicine, Journal Year: 2022, Volume and Issue: 181, P. 154 - 165

Published: Feb. 8, 2022

Language: Английский

---

Reactive Oxygen Species and NRF2 Signaling, Friends or Foes in Cancer?

Biomolecules, Journal Year: 2023, Volume and Issue: 13(2), P. 353 - 353

Published: Feb. 11, 2023

The imbalance between reactive oxygen species (ROS) production and clearance causes oxidative stress ROS, which play a central role in regulating cell tissue physiology pathology. Contingent upon concentration, ROS influence cancer development contradictory ways, either stimulating survival growth or causing death. Cells developed evolutionarily conserved programs to sense adapt redox the fluctuations regulate as signaling molecules toxic insults. transcription factor nuclear erythroid 2-related 2 (NRF2)-KEAP1 system is master regulator of cellular metabolic homeostasis. NRF2 has Janus-like roles carcinogenesis development. Short-term activation suppresses injury, inflammation, initiation. However, cells often exhibit constitutive due genetic mutations oncogenic signaling, conferring advantages for cells' growth. Emerging evidence suggests that hyperactivation, an adaptive phenotype under stressful tumor environments, regulates all hallmarks cancer. In this review, we summarized source regulation sensors (O2), reviewed recent progress on generation with focus new functions reach beyond what originally envisioned, including metabolism, autophagy, macropinocytosis, unfolded protein response, proteostasis, circadian rhythm, which, together anti-oxidant drug detoxification enzymes, contributes development, metastasis, anticancer therapy resistance.

Language: Английский

---

Mitochondrial Dysfunction: The Hidden Player in the Pathogenesis of Atherosclerosis?

International Journal of Molecular Sciences, Journal Year: 2023, Volume and Issue: 24(2), P. 1086 - 1086

Published: Jan. 6, 2023

Atherosclerosis is a multifactorial inflammatory pathology that involves metabolic processes. Improvements in therapy have drastically reduced the prognosis of cardiovascular disease. Nevertheless, significant residual risk still relevant, and related to unmet therapeutic targets. Endothelial dysfunction lipid infiltration are primary causes atherosclerotic plaque progression. In this contest, mitochondrial can affect arterial wall cells, particular macrophages, smooth muscle lymphocytes, endothelial causing an increase reactive oxygen species (ROS), leading oxidative stress, chronic inflammation, intracellular deposition. The detection characterization DNA (mtDNA) crucial for assessing defects should be considered goal new future interventions. review, we will focus on idea, based analysis data from many research groups, namely link between impairment and, particular, its effect atherosclerosis aging. Therefore, discuss known novel mitochondria-targeting therapies contest atherosclerosis.

Language: Английский

---

Oxidative Stress, Endoplasmic Reticulum Stress and Apoptosis in the Pathology of Alzheimer’s Disease

Cell Biochemistry and Biophysics, Journal Year: 2024, Volume and Issue: 82(2), P. 457 - 477

Published: March 12, 2024

Language: Английский

---

Expanding the Frontiers of Guardian Antioxidant Selenoproteins in Cardiovascular Pathophysiology

Antioxidants and Redox Signaling, Journal Year: 2024, Volume and Issue: 40(7-9), P. 369 - 432

Published: Feb. 1, 2024

Physiological levels of reactive oxygen and nitrogen species (ROS/RNS) function as fundamental messengers for many cellular developmental processes in the cardiovascular system. ROS/RNS involved cardiac redox-signaling originate from diverse sources, their are tightly controlled by key endogenous antioxidant systems that counteract accumulation. However, dysregulated redox-stress resulting inefficient removal leads to inflammation, mitochondrial dysfunction, cell death, contributing development progression disease (CVD).

Language: Английский

---

Polyphenols as Antioxidants for Extending Food Shelf-Life and in the Prevention of Health Diseases: Encapsulation and Interfacial Phenomena

Biomedicines, Journal Year: 2021, Volume and Issue: 9(12), P. 1909 - 1909

Published: Dec. 14, 2021

Toxicity caused by the exposure to human-made chemicals and environmental conditions has become a major health concern because they may significantly increase formation of reactive oxygen species (ROS), negatively affecting endogenous antioxidant defense. Living systems have evolved complex mechanisms protect cells from oxidative conditions. Although stress contributes various pathologies, intake molecules such as polyphenols, obtained natural sources, limit their effects antimicrobial properties against lipid peroxidation broad range foodborne pathogens. Ingestion polyphenol-rich foods, fruits vegetables, help reduce harmful ROS, but use supramolecular nanomaterials delivery emerged an efficient method improve pharmacological therapeutic effects. Suitable exogenous polyphenolic antioxidants should be readily absorbed delivered sites where pathological damage take place, for instance, intracellular locations. Many potential poor bioavailability, can encapsulated ideal solubility permeability profile. Development effective strategies requires creation new nanoscale drug stress. In this review we provide overview process, highlight some discuss role polyphenols bioactives in controlling overproduction ROS bacterial fungal growth, paying special attention encapsulation suitable location colloidal interfaces play crucial role.

Language: Английский

---

Ccl3 enhances docetaxel chemosensitivity in breast cancer by triggering proinflammatory macrophage polarization

Journal for ImmunoTherapy of Cancer, Journal Year: 2022, Volume and Issue: 10(5), P. e003793 - e003793

Published: May 1, 2022

Although the antitumor efficacy of docetaxel (DTX) has long been attributed to antimitotic activities, its impact on tumor microenvironment (TME) recently gained more attention. Macrophages are a major component TME and play critical role in DTX efficacy; however, underlying action mechanisms remain unclear.DTX chemotherapeutic was demonstrated via both macrophage depletion C-C motif chemokine ligand 3 (Ccl3)-knockout transgenic allograft mouse model. Ccl3-knockdown Ccl3-overexpressing breast cancer cell allografts were used for vivo study. Combination therapy evaluate effect Ccl3 induction chemosensitivity. Vital regulatory molecules pathways identified using RNA sequencing. Macrophage phagocytosis cells influence proliferation under treatment assessed an vitro coculture assay. Serum samples from patients with demonstrate clinical relevance our study.Our study revealed that induced by macrophages indispensable DTX. DTX-induced promoted proinflammatory polarization subsequently facilitated stem cells. overexpression suppress progression increase Mechanistically, relieving inhibition cAMP-response element binding protein reactive oxygen species accumulation, then activation Ccl3-C-C receptor 5-p38/interferon factor 5 pathway. High CCL3 expression predicted better prognosis, high chemosensitivity cancer. Furthermore, Creb inhibitor recombinant significantly enhanced chemosensitivity.Our results indicate triggers facilitates combination may provide promising therapeutic rationale increasing

Language: Английский

---

Integrated technologies for continuous monitoring of organs-on-chips: Current challenges and potential solutions

Biosensors and Bioelectronics, Journal Year: 2023, Volume and Issue: 224, P. 115057 - 115057

Published: Jan. 2, 2023

Language: Английский

---

Oxidative Stress and MicroRNAs in Endothelial Cells under Metabolic Disorders

Cells, Journal Year: 2023, Volume and Issue: 12(9), P. 1341 - 1341

Published: May 8, 2023

Reactive oxygen species (ROS) are radical intermediates that serve as important second messengers in signal transduction. However, when the accumulation of these molecules exceeds buffering capacity antioxidant enzymes, oxidative stress and endothelial cell (EC) dysfunction occur. EC shifts vascular system into a pro-coagulative, proinflammatory state, thereby increasing risk developing cardiovascular (CV) diseases metabolic disorders. Studies have turned to investigation microRNA treatment for CV factors, post-transcription regulators known co-regulate ROS. In this review, we will discuss ROS pathways generation, normal physiology ROS-induced dysfunction, current knowledge common disorders their connection stress. Therapeutic strategies based on microRNAs response microRNA’s regulatory roles controlling also be explored. It is gain an in-depth comprehension mechanisms generating how manipulating enzymatic byproducts can protect function from prevent development

Language: Английский

---