Disruption of cellular iron homeostasis by SRPX2-IRP1 interaction aggravates renal fibrosis in chronic kidney disease.

Pei-Ran Yin Lu-Miao Chen M. Ding Zhao-Nan Wei An-Ran Huo Yin-Fang Wang Meng-Jun Xie Hu Zhang Yuan Qin H. Ding Ying Lu Yan Shi Xun Zhou Qian-Sen Zhang Pan Fang K. Song Qi-Fei Cong

Sep 2026 · Cell Death and Differentiation · 0 citations · 64 references

Medicine

TL;DR

Findings reveal SRPX2 as a key pathogenic factor driving renal fibrosis by disrupting tubular iron homeostasis and Targeting the SRPX2-IRP1 regulatory axis presents a promising therapeutic strategy for slowing CKD progression.

DOI PubMed Semantic Scholar

View source

Similar papers

Open access Aug 2026

Mfn2-related mitochondrial dysfunction regulates renal fibrosis through ferroptosis in chronic kidney disease.

This study is the first to illustrate the role and relationship of mitochondrial dysfunction, especially mitophagy, and ferroptosis in renal fibrosis and their interaction with Mfn2, providing new insights and potential therapeutic targets for renal fibrosis.

Mingyu Zhang, Jingyu Wang, Ying Yang et al. · Biochimica et Biophysica Act... · 0 citations

Aug 2026

Remodeling lipid and mitochondrial homeostasis: a novel mechanism by which polydatin attenuates renal tubular senescence in chronic kidney disease.

PD rewires lipid metabolism, restores mitochondrial homeostasis, and activates the SIRT3/SOD2 axis to mitigate DNA damage and suppress tubular senescence, thereby halting CKD progression and position PD as a promising therapeutic candidate for senescence-associated kidney diseases.

Ting-Ting Wang, Hui Wang, Wenfeng Guo et al. · International Immunopharmaco... · 0 citations

Review Sep 2026

MicroRNAs in Renal Fibrosis: Unraveling Mechanisms and Therapeutic Potential.

Chronic Kidney Disease (CKD) poses a growing global health burden, with increasing prevalence driven by risk factors such as aging, metabolic disorders, and environmental influences. As CKD progresses, it frequently leads to renal fibrosis, a pathological condition characterized by excessive extracellular matrix (ECM)...

A. Doghish, Khaled Abuelhaded, M. M. Abdelaziz et al. · International Journal of Bio... · 0 citations

Open access Sep 2026

A novel Keap1-Nrf2 inhibitor 6K delays the progression of AKI-to-CKD by mitigating maladaptive repair

It is demonstrated that Nrf2 deficiency exacerbates AKI-CKD progression through redox imbalance and ferroptosis-mediated maladaptive repair, and targeting Keap1-Nrf2 with 6K protects against renal injury and fibrosis, highlighting its therapeutic potential for kidney diseases.

Yi-Ming Wang, Yi Sun, Ting Zhou et al. · Redox Biology · 0 citations

Open access Sep 2026

Targeting tubular NAT10 ameliorates the renal Tubulointerstitial Fibrosis in Obstructive and Folic Acid-Induced Nephropathy

Renal tubulointerstitial fibrosis (TIF) represents a common pathological hallmark during the progression of chronic kidney disease (CKD). NAT10, an RNA acetyltransferase, catalyzes N4-acetylcytidine modification of mRNA and has been associated with multiple pathological events, including bladder cancer progression, tum...

Qin Kang, Lin Yin, Chen Wu et al. · International Journal on Bio... · 0 citations

Sep 2026

Translocator Protein and Mitochondrial Dysfunction in Chronic Kidney Disease.

BACKGROUND Dysregulation of mitochondrial homeostasis is associated with kidney tubular injury and subsequent tubulointerstitial fibrosis, contributing to the development of chronic kidney diseases (CKD). Translocator protein (TSPO), located on the outer mitochondrial membrane, is upregulated in kidney tubules after in...

Yu-Chen Feng, W. Yiu, D. Lam et al. · Journal of the American Soci... · 0 citations