Mitochondria and cell death-associated inflammation

Vringer, Esmee; Tait, Stephen W.G.

doi:10.1038/s41418-022-01094-w

Cited by 113 publications

(74 citation statements)

References 120 publications

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“…It was found that the synthesized berberines did not affect the mitochondrial membrane potential ( Ψ m ) in isolated rat liver mitochondria, suggesting no negative impact on the functioning of organelles crucial to cell viability. 86–88 Furthermore, these investigated compounds did not influence the survival of both normal (HEK-293) and tumor-derived SH-SY5Y cells (IC 50 > 0.1 mM).…”

Section: Resultsmentioning

confidence: 91%

Optimal synthesis conditions for NBF-modified 8,13-dihydroberberine derivatives

Zagrebaev,

Butova,

Guda

et al. 2024

New J. Chem.

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Section: Resultsmentioning

confidence: 91%

Optimal synthesis conditions for NBF-modified 8,13-dihydroberberine derivatives

Zagrebaev,

Butova,

Guda

et al. 2024

New J. Chem.

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“…Mitochondrial dysfunction and associated excessive levels of mtROS are major supporters of inflammation [ 32 ] that drive the pathogenesis of many diseases, including neurodegenerative disorders, cancer, viral and bacterial infections, cardiovascular diseases, metabolic syndromes, and autoimmune disorders [ 31 ].…”

Section: Inflammation: An Overviewmentioning

confidence: 99%

Inflammation, Mitochondria and Natural Compounds Together in the Circle of Trust

Nesci

Spagnoletta

Oppedisano

2023

IJMS

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Human diseases are characterized by the perpetuation of an inflammatory condition in which the levels of Reactive Oxygen Species (ROS) are quite high. Excessive ROS production leads to DNA damage, protein carbonylation and lipid peroxidation, conditions that lead to a worsening of inflammatory disorders. In particular, compromised mitochondria sustain a stressful condition in the cell, such that mitochondrial dysfunctions become pathogenic, causing human disorders related to inflammatory reactions. Indeed, the triggered inflammation loses its beneficial properties and turns harmful if dysregulation and dysfunctions are not addressed. Thus, reducing oxidative stress with ROS scavenger compounds has proven to be a successful approach to reducing inflammation. Among these, natural compounds, in particular, polyphenols, alkaloids and coenzyme Q10, thanks to their antioxidant properties, are capable of inhibiting the activation of NF-κB and the expression of target genes, including those involved in inflammation. Even more, clinical trials, and in vivo and in vitro studies have demonstrated the antioxidant and anti-inflammatory effects of phytosomes, which are capable of increasing the bioavailability and effectiveness of natural compounds, and have long been considered an effective non-pharmacological therapy. Therefore, in this review, we wanted to highlight the relationship between inflammation, altered mitochondrial oxidative activity in pathological conditions, and the beneficial effects of phytosomes. To this end, a PubMed literature search was conducted with a focus on various in vitro and in vivo studies and clinical trials from 2014 to 2022.

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“…Inflammasomemediated and redox-sensitive inflammatory pathways act synergistically, potentially potentiating the inflammatory response. [114,115] Fujioka et al found that secondary inflammatory responses may be a potential therapeutic target for preventing damage caused by acute mitochondrial dysfunction in the lateral wall of the cochlea in rats. [116] As mentioned above, inflammation is the body's defensive response to stimuli to maintain homeostasis.…”

Section: Inflammation Dna Damage and Mitochondrial Imbalancementioning

confidence: 99%

Understanding the role of inflammation in sensorineural hearing loss: Current goals and future prospects

Li,

Chen,

Lin

et al. 2023

Brain-X

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Sensorineural hearing loss (SNHL) is a common otologic condition caused by damage to hair cells and spiral ganglion neurons that affects transmission pathways. Most of these cells cannot be regenerated, and there has been no breakthrough in regeneration techniques for inner ear cells. SNHL has a high incidence rate and can cause a variety of clinical symptoms, greatly impacting people's daily lives. With limited clinical treatments, the search for critical targets is urgent. Studies have shown that inflammation is prevalent in the pathogenesis of SNHL and plays a significant role in it. Inflammation is a normal body defense response, and a systemic anti‐inflammatory approach is undesirable. It is crucial for us to identify potential targets of inflammation in SNHL and take measures specifically targeting those targets with minimal systemic impact. This paper firstly describes the role of inflammation in various types of SNHL and then provides an overview of the interactions between inflammation and cochlear immunity, cochlear microcirculation, vascular spasm, and glutamate metabolism and finally comprehensively examines the feasibility of targets in these interactions. This paper is expected to facilitate the development of targeted anti‐inflammation for SNHL and provide strategies and approaches for treating clinical SNHL.

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Mitochondria and cell death-associated inflammation

Cited by 113 publications

References 120 publications

Optimal synthesis conditions for NBF-modified 8,13-dihydroberberine derivatives

Optimal synthesis conditions for NBF-modified 8,13-dihydroberberine derivatives

Inflammation, Mitochondria and Natural Compounds Together in the Circle of Trust

Understanding the role of inflammation in sensorineural hearing loss: Current goals and future prospects

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