Ferroptosis involves in renal tubular cell death in diabetic nephropathy

Wang, Yue; Bi, Ran; Quan, Fei; Cao, Qiu-Hua; Lin, Yining; Yue, Chongxiu; Cui, Xinmeng; Yang, Hongbao; Gao, Xinghua; Zhang, Dayong

doi:10.1016/j.ejphar.2020.173574

Cited by 146 publications

(143 citation statements)

References 34 publications

Supporting

Mentioning

120

Contrasting

Order By: Relevance

“…Previous studies have highlighted the importance of ferroptosis in the development of DN as inhibition of ferroptosis can effectively delay the progression of DN ( 18 , 19 ). It is reported that salusin-β serves as an inducer of oxidative stress in HK-2 cells through increased ROS levels and decreased GSH activities ( 35 ), key characteristics of ferroptosis ( 15 , 49 ).…”

Section: Resultsmentioning

confidence: 99%

“…Studies have demonstrated that ferroptosis is involved in the pathogenesis of inflammation, types of cancer, neurodegeneration and tissue injury ( 11 , 12 ). Emerging evidence has shown that ferroptosis is observed in several renal diseases, including nephrotoxic folic acid-induced acute kidney injury ( 13 ), rhabdomyolysis-induced renal damage ( 14 ), renal ischaemia-reperfusion injury ( 15 ), obesity-related kidney injury ( 16 ), carbon tetrachloride-induced renal toxicity ( 17 ) and DN ( 18 , 19 ). These findings suggest that modulation of ferroptosis may function as a future direction in the treatment of chronic or acute kidney injury.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Salusin‑β participates in high glucose‑induced HK‑2 cell ferroptosis in a Nrf‑2‑dependent manner

et al. 2021

View full text Add to dashboard Cite

Ferroptosis is critically involved in the pathophysiology of diabetic nephropathy (DN). As a bioactive peptide, salusin-β is abundantly expressed in the kidneys. However, it is unclear whether salusin-β participates in the pathologies of diabetic kidney damage by regulating ferroptosis. The present study found that high glucose (HG) treatment upregulated the protein expressions of salusin-β in a dose-and time-dependent manner. Genetic knockdown of salusin-β retarded, whereas overexpression of salusin-β aggravated, HG-triggered iron overload, antioxidant capability reduction, massive reactive oxygen species production and lipid peroxidation in HK-2 cells. Mechanistically, salusin-β inactivated nuclear factor erythroid-derived 2-like 2 (Nrf-2) signaling, thus contributing to HG-induced ferroptosis-related changes in HK-2 cells. Notably, the protein expression of salusin-β was upregulated by ferroptosis activators, such as erastin, RSL3, FIN56 and buthionine sulfoximine. Pretreatment with ferrostatin-1 (a ferroptosis inhibitor) prevented the upregulated protein expression of salusin-β in HK-2 cells exposed to HG. Taken together, these results suggested that a positive feedback loop between salusin-β and ferroptosis primes renal tubular cells for injury in diabetes.

show abstract

Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Salusin‑β participates in high glucose‑induced HK‑2 cell ferroptosis in a Nrf‑2‑dependent manner

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Direct studies regarding DN and ferroptosis were the first to be conducted in all types of CKD. The involvement of ferroptosis has been confirmed in streptozotocin-induced DN animal models [ 142 ]. To our knowledge, this is the first time that ferroptosis-specific mitochondrial changes in DN mice have been observed using transmission electron microscopy.…”

Section: Ferroptosis and Ckdmentioning

confidence: 99%

The Cross‐Link between Ferroptosis and Kidney Diseases

Wang

Liu

Wang

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

Acute and chronic kidney injuries result from structural dysfunction and metabolic disorders of the kidney in various etiologies, which significantly affect human survival and social wealth. Nephropathies are often accompanied by various forms of cell death and complex microenvironments. In recent decades, the study of kidney diseases and the traditional forms of cell death have improved. Nontraditional forms of cell death, represented by ferroptosis and necroptosis, have been discovered in the field of kidney diseases, which have reshuffled the role of traditional cell death in nephropathies. Although interactions between ferroptosis and acute kidney injury (AKI) have been continuously explored, studies on ferroptosis and chronic kidney disease (CKD) remain limited. Here, we have reviewed the therapeutic significance of ferroptosis in AKI and anticipated the curative potential of ferroptosis for CKD in the hope of providing insights into ferroptosis and CKD.

show abstract

“…Until fairly recently, researchers demonstrated that kidney tubular cell death in DN is related to ferroptosis based on the observation of declining expression of system Xc-and GPX4 mRNA and the enhancive ROS and lipid oxidation in vivo and in vitro respectively, which can be ameliorated by ferrostatin-1 (Fer-1) (Wang et al, 2020e;Kim et al, 2021;Li S. et al, 2021), implicating the positive curative effect to hinder ferroptosis. A recent study revealed the mechanism, which may have evinced HO-1 regulated by hypoxia-inducible factor (HIF), administering to iron accumulation by decomposing heme, resulting in the induction of ferroptosis to harm renal tubular in db/db mice (Feng et al, 2021), but detailing the pathophysiological process merits further investigation.…”

Section: Diabetic Nephropathy (Dn)mentioning

confidence: 99%

Ferroptosis and Its Potential Role in Metabolic Diseases: A Curse or Revitalization?

Duan

Lin

et al. 2021

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Ferroptosis is classified as an iron-dependent form of regulated cell death (RCD) attributed to the accumulation of lipid hydroperoxides and redox imbalance. In recent years, accumulating researches have suggested that ferroptosis may play a vital role in the development of diverse metabolic diseases, for example, diabetes and its complications (e.g., diabetic nephropathy, diabetic cardiomyopathy, diabetic myocardial ischemia/reperfusion injury and atherosclerosis [AS]), metabolic bone disease and adrenal injury. However, the specific physiopathological mechanism and precise therapeutic effect is still not clear. In this review, we summarized recent advances about the development of ferroptosis, focused on its potential character as the therapeutic target in metabolic diseases, and put forward our insights on this topic, largely to offer some help to forecast further directions.

show abstract

Ferroptosis involves in renal tubular cell death in diabetic nephropathy

Cited by 146 publications

References 34 publications

Salusin‑β participates in high glucose‑induced HK‑2 cell ferroptosis in a Nrf‑2‑dependent manner

Salusin‑β participates in high glucose‑induced HK‑2 cell ferroptosis in a Nrf‑2‑dependent manner

The Cross‐Link between Ferroptosis and Kidney Diseases

Ferroptosis and Its Potential Role in Metabolic Diseases: A Curse or Revitalization?

Contact Info

Product

Resources

About