Metabolic Chaos in Kidney Disease: Unraveling Energy Dysregulation DOI Open Access
Priya Gupta,

Saiya Zhu,

Yuan Gui

et al.

Journal of Clinical Medicine, Journal Year: 2024, Volume and Issue: 13(22), P. 6772 - 6772

Published: Nov. 11, 2024

Acute kidney injury (AKI) and chronic disease (CKD) share a fundamental disruption: metabolic dysfunction.

Language: Английский

Renal tubular epithelial IGFBP7 interacts with PKM2 to drive renal lipid accumulation and fibrosis DOI
Ju-tao Yu, Shuai-shuai Xie, Xiaoyu Shen

et al.

Molecular Therapy, Journal Year: 2025, Volume and Issue: unknown

Published: May 1, 2025

Language: Английский

Citations

0

Targeting pyruvate kinase M2 for the treatment of kidney disease DOI Creative Commons
Dan‐Qian Chen,

Jin Han,

Hongxing Liu

et al.

Frontiers in Pharmacology, Journal Year: 2024, Volume and Issue: 15

Published: June 7, 2024

Pyruvate kinase M2 (PKM2), a rate limiting enzyme in glycolysis, is cellular regulator that has received extensive attention and regards as metabolic of metabolism energy. Kidney highly metabolically active organ, glycolysis the important energy resource for kidney. The accumulated evidences indicates enzymatic activity PKM2 disturbed kidney disease progression treatment, especially diabetic acute injury. Modulating post-translational modification determines its nuclear translocation serves an interventional approach to regulate PKM2. Emerging show participate treatment through modulating regulation, podocyte injury, fibroblast activation proliferation, macrophage polarization, T cell regulation. Interestingly, activators (TEPP-46, DASA-58, mitapivat, TP-1454) inhibitors (shikonin, alkannin, compound 3k 3h) have exhibited potential therapeutic property disease, which pleiotropic effects In future, deep investigation urgently needed determine effect activator/inhibitor benefit patients. information this review highlights functions biomarker target diseases.

Language: Английский

Citations

3

N6-methyladenosine regulates metabolic remodeling in kidney aging through transcriptional regulator GLIS1 DOI Creative Commons
Xu Li, Shuo Chen, Qiuling Fan

et al.

BMC Biology, Journal Year: 2024, Volume and Issue: 22(1)

Published: Dec. 31, 2024

Age-related kidney impairment, characterized by tubular epithelial cell senescence and renal fibrosis, poses a significant global public health threat. Although N6-methyladenosine (m6A) methylation is implicated in various pathological processes, its regulatory mechanism aging remains unclear. An m6A-mRNA epitranscriptomic microarray was performed to identify genes with abnormal m6A modifications aged human tissues. Histological, immunohistochemical, immunofluorescent staining, western blot, RT-qPCR were employed examine the biological functions of targeted methyltransferases both vivo vitro. RNA immunoprecipitation, chromatin ribosomal luciferase reporter assays used investigate specific interactions between methyltransferases, genes, their downstream signals. Significantly lower modification levels observed GLIS1, identified as "metabolic remodeling factor," showed significantly reduced protein modifications. The downregulation GLIS1 induced fibrosis shifting metabolic from fatty acid oxidation (FAO) glycolysis. Additionally, methylated mRNA regulated expression METTL3 YTHDF1. Silencing METTL3/YTHDF1 weakened translation disrupted balance FAO Our findings suggest that activated YTHDF1-dependent manner, leads regulating shift This provides promising therapeutic target for aging.

Language: Английский

Citations

1

CircRNA-0013747 induces mesangial cell proliferation in IgA nephropathy by targeting the Warburg effect via miR-330- 3p/PKM2 signaling DOI Creative Commons
Huimei Zou, Peilei Chen,

Wenli Deng

et al.

Research Square (Research Square), Journal Year: 2024, Volume and Issue: unknown

Published: March 5, 2024

Abstract Aberrant mesangial cell proliferation is a prevailing histopathological feature of immunoglobulin A nephropathy (IgAN) and the primary driver glomerular sclerosis impaired renal function in IgAN patients. Prior research has revealed that PKM2-mediated aerobic glycolysis (the Warburg effect) frequently promotes growth contributes to development various acute chronic kidney diseases. However, expression functionality PKM2 IgA nephropathy, as well underlying molecular mechanisms governing its abnormal expression, remain elusive. Circular RNAs, subset noncoding have garnered increasing attention due mounting evidence their pivotal roles initiation progression numerous disorders. The present study aimed explore effects circRNA_0013747 on potential mechanisms. results indicated notable overexpression lipopolysaccharide (LPS)-treated human cells (HMCs) biopsy samples from CircRNA_0013747 was shown facilitate activate glycolysis, although these were mitigated by an increase miR-330-3p. Mechanistically, physically interacted with microRNA-330-3p (miR-330-3p) hindered directly binding it. These findings imply can enhance modulating miR-330-3p/PKM2 signaling pathway. In conclusion, underscore possibility serving promising therapeutic target for IgAN, suggesting new prospects treating this disease.

Language: Английский

Citations

0

Compound 3K attenuates isoproterenol-induced cardiac hypertrophy by inhibiting pyruvate kinase M2 (PKM2) pathway DOI
Mohd Rihan, Shyam Sunder Sharma

Life Sciences, Journal Year: 2024, Volume and Issue: 351, P. 122837 - 122837

Published: June 13, 2024

Language: Английский

Citations

0

Transcriptomics of tissue exosomes to investigate miR-195-5p’s amelioration of endometrial fibrosis via the YAP-Smad7 pathway: an animal study DOI Creative Commons

Jia‐ming Chen,

Qiao-yi Huang,

Weihong Chen

et al.

Journal of Translational Medicine, Journal Year: 2024, Volume and Issue: 22(1)

Published: Nov. 21, 2024

A significant research gap exists regarding the role of tissue exosomes in intrauterine adhesions (IUAs). This study aims to investigate involvement miR-195-5p and its regulatory network IUAs through analysis exosomes. Exosomes from rat uterine with were analyzed via transcriptomics identify downstream target genes miR-195-5p, cross-referencing human endometrial database GSE224093. Dual luciferase labeling confirmed miRNA-target gene interactions. The therapeutic efficacy a agonist was assessed vivo HE staining, Masson mating tests. mechanisms underlying extracellular matrix (ECM) deposition myofibroblast transdifferentiation fibrosis investigated both vitro using RT-PCR, Western Blot, immunofluorescence, immunohistochemistry. Migration ability stromal cells evaluated CCK8, scratch tests, Transwell assays. Finally, clinical potential compared autologous adipose-derived mesenchymal stem cells. expression found be decreased. Treatment resulted improved health, reduced fibrosis, increased glandular density, enhanced birth rates rats. Both experiments that decreased ECM deposition, transdifferentiation, inhibited migration achieved downregulation YAP Hippo pathway upregulation Smad7. Notably, agonists comparable cell therapy, offering promising avenues for application. Differential can reduce improving by regulating YAP-Smad7 signaling cascade.

Language: Английский

Citations

0

Inhibition of PKM2 by shikonin impedes TGF-β1 expression by repressing histone lactylation to alleviate renal fibrosis DOI

Tianya Xiang,

Xijian Wang,

Shujiao Huang

et al.

Phytomedicine, Journal Year: 2024, Volume and Issue: 136, P. 156324 - 156324

Published: Dec. 15, 2024

Language: Английский

Citations

0

T cell metabolism in kidney immune homeostasis DOI Creative Commons
Zhirong Liu,

Binbin Dai,

Jiwen Bao

et al.

Frontiers in Immunology, Journal Year: 2024, Volume and Issue: 15

Published: Dec. 16, 2024

Kidney immune homeostasis is intricately linked to T cells. Inappropriate differentiation, activation, and effector functions of cells lead a spectrum kidney disease. While executing functions, undergo series metabolic rewiring meet the rapid energy demand. The key enzymes metabolites involved in cell metabolism metabolically epigenetically modulate cells' thereby being capable modulating homeostasis. In this review, we first summarize latest advancements immunometabolism. Second, outline alterations renal microenvironment under certain disease conditions. Ultimately, highlight modulation within homeostasis, which may shed light on new strategies for treating

Language: Английский

Citations

0

Metabolic Chaos in Kidney Disease: Unraveling Energy Dysregulation DOI Open Access
Priya Gupta,

Saiya Zhu,

Yuan Gui

et al.

Journal of Clinical Medicine, Journal Year: 2024, Volume and Issue: 13(22), P. 6772 - 6772

Published: Nov. 11, 2024

Acute kidney injury (AKI) and chronic disease (CKD) share a fundamental disruption: metabolic dysfunction.

Language: Английский

Citations

0