Lipin-1 deficiency deteriorates defect of fatty acid β-oxidation and lipid-related kidney damage in diabetic kidney disease

Lin, Simei; Wang, Liang; Jia, Yingli; Sun, Ying; Qiao, Panshuang; Quan, Yazhu; Liu, J; Hu, Huihui; Yang, Baoxue; Zhou, Hong

doi:10.1016/j.trsl.2023.07.004

Cited by 4 publications

(2 citation statements)

References 56 publications

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“…Lipin-1 inhibits adipose synthesis, upregulates FAO, attenuates proximal tubular epithelial cell injury in tubulointerstitial fibrosis, and delays DKD by promoting proliferator-activated receptor-gamma co-activator-1alpha(PGC-1α)/PPARα-mediated Carnitine Palmitoyltransferase 1 Alpha(Cpt1α)/hepatocyte nuclear factor 4alpha signaling and upregulating SREBPs ( 194 ).…”

Section: Targeting Lipid Metabolism For Dkd Treatmentmentioning

confidence: 99%

Lipid metabolism disorder in diabetic kidney disease

Han,

Du,

Zhu

et al. 2024

Front. Endocrinol.

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Diabetic kidney disease (DKD), a significant complication associated with diabetes mellitus, presents limited treatment options. The progression of DKD is marked by substantial lipid disturbances, including alterations in triglycerides, cholesterol, sphingolipids, phospholipids, lipid droplets, and bile acids (BAs). Altered lipid metabolism serves as a crucial pathogenic mechanism in DKD, potentially intertwined with cellular ferroptosis, lipophagy, lipid metabolism reprogramming, and immune modulation of gut microbiota (thus impacting the liver-kidney axis). The elucidation of these mechanisms opens new potential therapeutic pathways for DKD management. This research explores the link between lipid metabolism disruptions and DKD onset.

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Section: Targeting Lipid Metabolism For Dkd Treatmentmentioning

confidence: 99%

Lipid metabolism disorder in diabetic kidney disease

Han,

Du,

Zhu

et al. 2024

Front. Endocrinol.

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“…Increased expression of SREBP-1 protein and concomitant lipid accumulation has been observed in both DKD patients and mouse models [ 43 ]. Liptin-1 deficiency in TECs can promote lipid synthesis and exacerbate renal tubulointerstitial fibrosis in DKD by inhibiting PGC-1α/PPARα and up-regulating SREBPs [ 44 ].…”

Section: Metabolic Reprogramming Of Dkdmentioning

confidence: 99%

Mitochondrial metabolic reprogramming in diabetic kidney disease

Fan,

Yang,

Lang

et al. 2024

Cell Death Dis

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Diabetic kidney disease, known as a glomerular disease, arises from a metabolic disorder impairing renal cell function. Mitochondria, crucial organelles, play a key role in substance metabolism via oxidative phosphorylation to generate ATP. Cells undergo metabolic reprogramming as a compensatory mechanism to fulfill energy needs for survival and growth, attracting scholarly attention in recent years. Studies indicate that mitochondrial metabolic reprogramming significantly influences the pathophysiological progression of DKD. Alterations in kidney metabolism lead to abnormal expression of signaling molecules and activation of pathways, inducing oxidative stress-related cellular damage, inflammatory responses, apoptosis, and autophagy irregularities, culminating in renal fibrosis and insufficiency. This review delves into the impact of mitochondrial metabolic reprogramming on DKD pathogenesis, emphasizing the regulation of metabolic regulators and downstream signaling pathways. Therapeutic interventions targeting renal metabolic reprogramming can potentially delay DKD progression. The findings underscore the importance of focusing on metabolic reprogramming to develop safer and more effective therapeutic approaches.

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