Targeting mitochondria in dermatological therapy: beyond oxidative damage and skin aging DOI
Tongyu C. Wikramanayake, Jérémy Chéret, Alec Sevilla

и другие.

Expert Opinion on Therapeutic Targets, Год журнала: 2022, Номер 26(3), С. 233 - 259

Опубликована: Март 4, 2022

Introduction The analysis of the role mitochondria in oxidative damage and skin aging has been a significant aspect dermatological research. Mitochondria generate most reactive oxygen species (ROS) which, excess, are cytotoxic DNA-damaging promote (photo-)aging. However, ROS also possesses key physiological regulatory functions mitochondrial dysfunction is prominent several not primarily senescence-associated diseases cancers. Although many standard dermatotherapeutics modulate function, therapy rarely targets mitochondria. Accordingly, there rationale for 'mitochondrial dermatology'-based approaches to be applied therapeutic research, as we advocate here.Areas covered This paper examines cutaneous physiology beyond energy (ATP) production. Keratinocyte differentiation epidermal barrier maintenance, appendage morphogenesis homeostasis, photoaging cancer considered. Based on related PubMed search results, evaluates thyroid hormones, glucocorticoids, Vitamin D3 derivatives, retinoids, cannabinoid receptor agonists, PPARγ thyrotropin, thyrotropin-releasing hormone instructive lead compounds. Moreover, protein MPZL3 promising new drug target future dermatology' highlighted.Expert opinion Future research should have medicine emphasis. Focusing selected agents, targets, silico design, model will fertilize mito-centric approach.

Язык: Английский

Copper-induced cell death DOI

Martha A. Kahlson,

Scott J. Dixon

Science, Год журнала: 2022, Номер 375(6586), С. 1231 - 1232

Опубликована: Март 17, 2022

Excess copper causes mitochondrial protein aggregation and triggers a distinct form of cell death.

Язык: Английский

Процитировано

347

The therapeutic potential of targeting regulated non-apoptotic cell death DOI
Kamyar Hadian, Brent R. Stockwell

Nature Reviews Drug Discovery, Год журнала: 2023, Номер 22(9), С. 723 - 742

Опубликована: Авг. 7, 2023

Язык: Английский

Процитировано

180

Metabolic cell death in cancer: ferroptosis, cuproptosis, disulfidptosis, and beyond DOI Creative Commons
Chao Mao, Min Wang, Li Zhuang

и другие.

Protein & Cell, Год журнала: 2024, Номер 15(9), С. 642 - 660

Опубликована: Фев. 29, 2024

Abstract Cell death resistance represents a hallmark of cancer. Recent studies have identified metabolic cell as unique forms regulated resulting from an imbalance in the cellular metabolism. This review discusses mechanisms death—ferroptosis, cuproptosis, disulfidptosis, lysozincrosis, and alkaliptosis—and explores their potential cancer therapy. Our underscores complexity pathways offers insights into innovative therapeutic avenues for treatment.

Язык: Английский

Процитировано

43

The Role of the Metabolism of Zinc and Manganese Ions in Human Cancerogenesis DOI Creative Commons
Julian M. Rozenberg, Мargarita Kamynina, Maxim Sorokin

и другие.

Biomedicines, Год журнала: 2022, Номер 10(5), С. 1072 - 1072

Опубликована: Май 5, 2022

Metal ion homeostasis is fundamental for life. Specifically, transition metals iron, manganese and zinc play a pivotal role in mitochondrial metabolism energy generation, anti-oxidation defense, transcriptional regulation the immune response. The misregulation of expression or mutations carriers corresponding changes Mn2+ Zn2+ levels suggest that these ions cancer progression. Moreover, coordinated have been detected, suggesting particular mechanisms influenced by both might be required growth cells, metastasis evasion. Here, we present review pathophysiology cooperatively regulate cancerogenesis. Zn Mn effects converge on mitochondria-induced apoptosis, cGAS-STING signaling pathway, mediating Both influence progression impact treatment efficacy animal models clinical trials. We predict novel strategies targeting will complement current therapeutic strategies.

Язык: Английский

Процитировано

48

Driving factors of neuronal ferroptosis DOI
Julie Jacquemyn, Isha Ralhan, Maria S. Ioannou

и другие.

Trends in Cell Biology, Год журнала: 2024, Номер 34(7), С. 535 - 546

Опубликована: Фев. 23, 2024

Язык: Английский

Процитировано

17

The ion channels of endomembranes DOI
Meiqin Hu, Xinghua Feng, Qiang Liu

и другие.

Physiological Reviews, Год журнала: 2024, Номер 104(3), С. 1335 - 1385

Опубликована: Март 7, 2024

The endomembrane system consists of organellar membranes in the biosynthetic pathway [endoplasmic reticulum (ER), Golgi apparatus, and secretory vesicles] as well those degradative (early endosomes, macropinosomes, phagosomes, autophagosomes, late lysosomes). These organelles/vesicles work together to synthesize, modify, package, transport, degrade proteins, carbohydrates, lipids, regulating balance between cellular anabolism catabolism. Large ion concentration gradients exist across endomembranes: Ca 2+ for most organelles H + acidic compartments. Ion (Na , K Cl − ) channels on control flux response cues, allowing rapid informational exchange cytosol organelle lumen. Recent advances proteomics, electrophysiology, luminal juxtaorganellar imaging have led molecular identification functional characterization about two dozen channels. For example, whereas IP3R1–3 mediate release from ER neurotransmitter hormone stimulation, TRPML1–3 TMEM175 lysosomal release, respectively, nutritional trafficking cues. This review aims summarize current understanding these channels, with a focus their subcellular localizations, permeation properties, gating mechanisms, cell biological functions, disease relevance.

Язык: Английский

Процитировано

13

Emerging mechanisms and promising approaches in pancreatic cancer metabolism DOI Creative Commons
Hao Wu,

Mengdi Fu,

Mengwei Wu

и другие.

Cell Death and Disease, Год журнала: 2024, Номер 15(8)

Опубликована: Авг. 1, 2024

Abstract Pancreatic cancer is an aggressive with a poor prognosis. Metabolic abnormalities are one of the hallmarks pancreatic cancer, and cells can adapt to biosynthesis, energy intake, redox needs through metabolic reprogramming tolerate nutrient deficiency hypoxic microenvironments. use glucose, amino acids, lipids as maintain malignant growth. Moreover, they also metabolically interact in tumour microenvironment change cell fate, promote progression, even affect immune responses. Importantly, changes at body level deserve more attention. Basic research clinical trials based on targeted therapy or combination other treatments full swing. A comprehensive in-depth understanding regulation will not only enrich mechanisms disease progression but provide inspiration for new diagnostic therapeutic approaches.

Язык: Английский

Процитировано

13

From ferroptosis to cuproptosis, and calcicoptosis, to find more novel metals-mediated distinct form of regulated cell death DOI
Jie Gu,

Chuanzhi Guo,

Jiacheng Ruan

и другие.

APOPTOSIS, Год журнала: 2024, Номер 29(5-6), С. 586 - 604

Опубликована: Фев. 7, 2024

Язык: Английский

Процитировано

12

The crosstalk between mitochondrial quality control and metal-dependent cell death DOI Creative Commons

Qi-yuan Zhou,

Chao Ren,

Jing‐Yan Li

и другие.

Cell Death and Disease, Год журнала: 2024, Номер 15(4)

Опубликована: Апрель 27, 2024

Abstract Mitochondria are the centers of energy and material metabolism, they also serve as storage dispatch hubs metal ions. Damage to mitochondrial structure function can cause abnormal levels distribution ions, leading cell dysfunction even death. For a long time, quality control pathways such dynamics mitophagy have been considered inhibit metal-induced However, with discovery new metal-dependent death including ferroptosis cuproptosis, increasing evidence shows that there is complex relationship between This article reviews latest research results mechanisms crosstalk in recent years, well their involvement neurodegenerative diseases, tumors other order provide ideas for treatment related diseases.

Язык: Английский

Процитировано

11

MCOLN1/TRPML1 in the lysosome: a promising target for autophagy modulation in diverse diseases DOI

Jiansong Qi,

Qingqing Li,

Tianli Xin

и другие.

Autophagy, Год журнала: 2024, Номер 20(8), С. 1712 - 1722

Опубликована: Март 24, 2024

MCOLN1/TRPML1 is a nonselective cationic channel specifically localized to the late endosome and lysosome. With its property of mediating release several divalent cations such as Ca2+, Zn2+ Fe2+ from lysosome cytosol, MCOLN1 plays pivotal role in regulating variety cellular events including endocytosis, exocytosis, lysosomal biogenesis, reformation, especially Macroautophagy/autophagy. Autophagy highly conserved catabolic process that maintains cytoplasmic integrity by removing superfluous proteins damaged organelles. Acting terminal compartments, lysosomes are crucial for completion autophagy process. This review delves into emerging controlling autophagic ionic homeostasis, thereby governing fundamental functions lysosomes. Furthermore, this summarizes physiological relevance well molecular mechanisms through which orchestrates autophagy, consequently influencing mitochondria turnover, cell apoptosis migration. In addition, we have illustrated implications MCOLN1-regulated pathological cancer myocardial ischemia-reperfusion (I/R) injury. summary, given involvement MCOLN1-mediated pathogenesis I/R injury, targeting May provide clues developing new therapeutic strategies treatment these diseases. Exploring regulation diverse diseases contexts will surely broaden our understanding pathway offer potential promising drug target.

Язык: Английский

Процитировано

10