Ferroptosis in lymphoma: Emerging mechanisms and a novel therapeutic approach

Zhou, Qiao; Li, Ting; Qin, Qin; Xiao-bo, Huang; Wang, Yi

doi:10.3389/fgene.2022.1039951

Cited by 9 publications

(5 citation statements)

References 85 publications

(104 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Within the mitochondria,

produced by the respiratory chain can enter the mitochondrial membrane and be converted into a potent oxidant known as the hydroxyl radical. This hydroxyl radical then oxidizes polyunsaturated fatty acids in the mitochondrial membranes, leading to the formation of lipid hydroperoxides (ROOH) [ 29 ].…”

Section: Ferroptosis and Lipid Peroxidation In Amimentioning

confidence: 99%

Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction

Wu,

Li,

Cheng

et al. 2024

Rev. Cardiovasc. Med.

View full text Add to dashboard Cite

Acute myocardial infarction (AMI) is triggered by the blockage of coronary arteries, leading to restricted blood flow to the myocardium, which results in damage and cell death. While the traditional understanding of cell death primarily revolves around apoptosis, a new player in the game has emerged: ferroptosis. This novel form of cell death relies on iron and is propelled by reactive oxygen species (ROS). Lipid metabolism, an indispensable physiological process, plays a vital role in preserving cellular homeostasis. However, when this metabolic pathway is disrupted, the accumulation of excess waste increases, specifically lipid peroxides, which are strongly linked to the occurrence and progression of AMI. As a result, comprehending this complex interaction between ferroptosis and lipid metabolism could pave the way for new therapeutic approaches in tackling AMI.

show abstract

“…Within the mitochondria,

Section: Ferroptosis and Lipid Peroxidation In Amimentioning

confidence: 99%

Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction

Wu,

Li,

Cheng

et al. 2024

Rev. Cardiovasc. Med.

View full text Add to dashboard Cite

show abstract

“…The second approach is targeting GPX4, such as RAS-selective lethal 3 (RSL3) and ML-162 (Shin et al, 2018;Sui et al, 2018;Li et al, 2021;Liu et al, 2022). The ferroptosis inhibitors, Fer-1 (Miotto et al, 2020;Sripetchwandee et al, 2023), lipoxstatin-1 (Yang et al, 2014;Shin et al, 2018;Fan et al, 2021), and 1,8-Diazafluoren-9-one (DFO) (Bruni et al, 2018;Zeng et al, 2022;Zhou et al, 2022), are the three most frequently used compounds (Table 1).…”

Section: Drugs For Ferroptosis and The Possibility Of Its Use In Alco...mentioning

confidence: 99%

Targeting ferroptosis, a novel programmed cell death, for the potential of alcohol-related liver disease therapy

Shi

Liu

Wang³

et al. 2023

Front. Pharmacol.

Self Cite

View full text Add to dashboard Cite

Ferroptosis is a new iron-dependent cell death mode, which is different from the other types of programmed cell death, such as apoptosis, necrosis, and autophagy. Ferroptosis is characterized by a process in which fatal lipids from lipid peroxidation accumulate in cells and eventually lead to cell death. Alcohol-related liver disease (ALD) is a type of liver injury caused by excessive alcohol intake. Alcohol-related liver disease is a broad-spectrum disease category, which includes fatty liver, steatohepatitis, hepatitis, cirrhosis, and hepatocellular tumors. Recent studies have found that ferroptosis is involved in the pathological development of non-viral liver diseases. Therefore, ferroptosis may be an ideal target for the treatment of non-viral liver diseases. In this review article, we will elaborate the molecular mechanism and regulatory mechanism of ferroptosis, explore the key role of ferroptosis in the Alcohol-related liver disease process, and summarize the existing targeted ferroptosis drugs and their feasibility for the treatment of Alcohol-related liver disease.

show abstract

“…In addition, dietary habits also affect the content of free unsaturated fatty acids (34). However, PUFA cannot directly cause ferroptosis (35), which needs to be further catalyzed by ACSL family members into phosphorylated PUFA (PUFA-PL), or lipid metabolism that also produces a small amount of PUFA-PL (36). PUFA-PL then enters the cytoplasm as a prelude to ferroptosis.…”

Section: Mechanism 2111 Source: Pufa-plmentioning

confidence: 99%

Ferroptosis, necroptosis and cuproptosis: Novel forms of regulated cell death in diabetic cardiomyopathy

Zhang

Liu

et al. 2023

Front. Cardiovasc. Med.

View full text Add to dashboard Cite

Diabetes is a common chronic metabolic disease, and its incidence continues to increase year after year. Diabetic patients mainly die from various complications, with the most common being diabetic cardiomyopathy. However, the detection rate of diabetic cardiomyopathy is low in clinical practice, and targeted treatment is lacking. Recently, a large number of studies have confirmed that myocardial cell death in diabetic cardiomyopathy involves pyroptosis, apoptosis, necrosis, ferroptosis, necroptosis, cuproptosis, cellular burial, and other processes. Most importantly, numerous animal studies have shown that the onset and progression of diabetic cardiomyopathy can be mitigated by inhibiting these regulatory cell death processes, such as by utilizing inhibitors, chelators, or genetic manipulation. Therefore, we review the role of ferroptosis, necroptosis, and cuproptosis, three novel forms of cell death in diabetic cardiomyopathy, searching for possible targets, and analyzing the corresponding therapeutic approaches to these targets.

show abstract

Ferroptosis in lymphoma: Emerging mechanisms and a novel therapeutic approach

Cited by 9 publications

References 85 publications

Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction

Ferroptosis and Lipid Metabolism in Acute Myocardial Infarction

Targeting ferroptosis, a novel programmed cell death, for the potential of alcohol-related liver disease therapy

Ferroptosis, necroptosis and cuproptosis: Novel forms of regulated cell death in diabetic cardiomyopathy

Contact Info

Product

Resources

About