Is mitochondrial morphology important for cellular physiology? DOI
Timothy Wai

Trends in Endocrinology and Metabolism, Journal Year: 2024, Volume and Issue: 35(10), P. 854 - 871

Published: June 12, 2024

Language: Английский

Ferroptotic therapy in cancer: benefits, side effects, and risks DOI Creative Commons
Jiandong Diao,

Yuanyuan Jia,

Enyong Dai

et al.

Molecular Cancer, Journal Year: 2024, Volume and Issue: 23(1)

Published: May 3, 2024

Abstract Ferroptosis is a type of regulated cell death characterized by iron accumulation and uncontrolled lipid peroxidation, leading to plasma membrane rupture intracellular content release. Originally investigated as targeted therapy for cancer cells carrying oncogenic RAS mutations, ferroptosis induction now exhibits potential complement chemotherapy, immunotherapy, radiotherapy in various types. However, it can lead side effects, including immune death, bone marrow impairment, liver kidney damage, cachexia (severe weight loss muscle wasting), secondary tumorigenesis. In this review, we discuss the advantages offer an overview diverse range documented effects. Furthermore, examine underlying mechanisms explore strategies effect mitigation.

Language: Английский

Citations

28

Apoptotic Bodies Derived from Fibroblast‐Like Cells in Subcutaneous Connective Tissue Inhibit Ferroptosis in Ischaemic Flaps via the miR‐339‐5p/KEAP1/Nrf2 Axis DOI Creative Commons

Gaoxiang Yu,

Yijie Chen, Ningning Yang

et al.

Advanced Science, Journal Year: 2024, Volume and Issue: 11(24)

Published: April 19, 2024

Abstract Preventing and treating avascular necrosis at the distal end of flaps are critical to surgery success, but current treatments not ideal. A recent study shows that apoptotic bodies (ABs) generated near site apoptosis can be taken up promote cell proliferation. The reveals ABs derived from fibroblast‐like cells in subcutaneous connective tissue (FSCT cells) skin promoted ischaemic flap survival. It is also found inhibited death oxidative stress M1‐to‐M2 polarization macrophages. Transcriptome sequencing protein level testing demonstrated survival endothelial macrophages by inhibiting ferroptosis via KEAP1‐Nrf2 axis. Furthermore, microRNA (miR) data vitro vivo experiments KEAP1 delivering miR‐339‐5p exert therapeutic effects. In conclusion, FSCT cell‐derived ferroptosis, macrophage transition miR‐339‐5p/KEAP1/Nrf2 axis These results provide a potential strategy administering ABs.

Language: Английский

Citations

18

OPA1 promotes ferroptosis by augmenting mitochondrial ROS and suppressing an integrated stress response DOI
Felix G. Liang, Fereshteh Zandkarimi, Jae‐Hoon Lee

et al.

Molecular Cell, Journal Year: 2024, Volume and Issue: 84(16), P. 3098 - 3114.e6

Published: Aug. 1, 2024

Language: Английский

Citations

16

Mitochondrial protein import stress DOI
Nikolaus Pfanner, Fabian den Brave, Thomas Becker

et al.

Nature Cell Biology, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 22, 2025

Language: Английский

Citations

3

Sodium aescinate-induced hepatotoxicity via ATF4/GSH/GPX4 axis-mediated ferroptosis DOI Creative Commons
Xi Chen, Jie Zhou, Xin Zheng

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 7, 2025

Sodium aescinate (SA), a natural plant extract with various bioactivities, is widely used to treat oedema and inflammation in clinics. However, adverse events, including liver injury, kidney phlebitis, have been reported patients SA recent years. In this study, we BALB/c mice L02 cells evaluate the role of ferroptosis SA-induced injury. significantly increased AST, ALT, MDA Fe2+, decreased GSH levels, induced pathological changes vivo. also reduced viability LDH release, intracellular cysteine reduction, depletion, iron accumulation, ROS production, lipid peroxidation, indicating that causes ferroptosis. addition, inhibited transcriptional activity activating transcription factor 4 (ATF4) subsequently expression downstream genes xCT (solute carrier family 7a member 11, SLC7A11) Cystathionine gamma-lyase (CTH) which play vital roles biosynthesis. Interestingly, cytotoxic effects were effectively attenuated by ATF4 overexpression, while they aggravated silencing. These results revealed triggers hepatocyte inhibiting ATF4, an oxidative imbalance.

Language: Английский

Citations

2

Mitohormesis DOI Creative Commons
Yu‐Wei Cheng, Jie Liu, Toren Finkel

et al.

Cell Metabolism, Journal Year: 2023, Volume and Issue: 35(11), P. 1872 - 1886

Published: Nov. 1, 2023

Language: Английский

Citations

39

DELE1 oligomerization promotes integrated stress response activation DOI
Jie Yang, Kelsey R. Baron,

Daniel E. Pride

et al.

Nature Structural & Molecular Biology, Journal Year: 2023, Volume and Issue: 30(9), P. 1295 - 1302

Published: Aug. 7, 2023

Language: Английский

Citations

30

Mitochondrial DNA breaks activate an integrated stress response to reestablish homeostasis DOI Creative Commons
Yi Fu, Olivia Sacco,

Emily DeBitetto

et al.

Molecular Cell, Journal Year: 2023, Volume and Issue: 83(20), P. 3740 - 3753.e9

Published: Oct. 1, 2023

Language: Английский

Citations

24

Mitochondrial quality control in health and cardiovascular diseases DOI Creative Commons
Asli E. Atici, Timothy R. Crother, Magali Noval Rivas

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2023, Volume and Issue: 11

Published: Nov. 6, 2023

Cardiovascular diseases (CVDs) are one of the primary causes mortality worldwide. An optimal mitochondrial function is central to supplying tissues with high energy demand, such as cardiovascular system. In addition producing ATP a power source, mitochondria also heavily involved in adaptation environmental stress and fine-tuning tissue functions. Mitochondrial quality control (MQC) through fission, fusion, mitophagy, biogenesis ensures clearance dysfunctional preserves homeostasis tissues. Furthermore, generate reactive oxygen species (ROS), which trigger production pro-inflammatory cytokines regulate cell survival. dysfunction has been implicated multiple CVDs, including ischemia-reperfusion (I/R), atherosclerosis, heart failure, cardiac hypertrophy, hypertension, diabetic genetic cardiomyopathies, Kawasaki Disease (KD). Thus, MQC pivotal promoting health. Here, we outline mechanisms discuss current literature on CVDs.

Language: Английский

Citations

24

Inhibition of CARM1‐Mediated Methylation of ACSL4 Promotes Ferroptosis in Colorectal Cancer DOI Creative Commons
Shengjie Feng,

Zejun Rao,

Jiakun Zhang

et al.

Advanced Science, Journal Year: 2023, Volume and Issue: 10(36)

Published: Nov. 9, 2023

Abstract Ferroptosis, which is caused by iron‐dependent accumulation of lipid peroxides, an emerging form regulated cell death and considered a potential target for cancer therapy. However, the regulatory mechanisms underlying ferroptosis remain unclear. This study defines distinctive role ferroptosis. Inhibition CARM1 can increase sensitivity tumor cells to inducers in vitro vivo. Mechanistically, it found that ACSL4 methylated at arginine 339 (R339). Furthermore, R339 methylation promotes RNF25 binding ACSL4, contributes ubiquitylation ACSL4. The blockade facilitates effectively enhances ferroptosis‐associated immunotherapy. Overall, this demonstrates critical contributor resistance highlights as candidate therapeutic improving effects ferroptosis‐based antitumor

Language: Английский

Citations

23