Adiponectin in renal fibrosis

Jing, Huan; Tang, Simin; Shi, Lin; Liao, Mengyang; Chen, Hongtao; Fan, Yu; Zhou, Jun

doi:10.18632/aging.102811

Cited by 24 publications

(12 citation statements)

References 83 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Activation of the AMPK pathway after the binding of APN to AdipoR1 inhibits its downstream pathway, significantly resisting stress, inhibiting protein synthesis, and preventing fibrosis [14,15]. Therefore, the AdipoR1-AMPK pathway plays an important role in maintaining the normal physiological homeostasis of the kidney [3]. The study confirmed that the APN decreased in patients with coronary artery disease and metabolic syndrome [16,17]; still, the APN was at a high level in different stages of CKD [18,19,20].…”

Section: Discussionmentioning

confidence: 60%

“…APN has the effects of insulinsensitizing, anti-inflammation, and anti-atherosclerosis. Some scholars have found that the AdipoR1-AMP-activated protein kinase (AMPK) pathway can maintain the normal physiological homeostasis of the kidney [3]. Serum uric acid (UA) is an independent predictor of the development, progress, and prognosis of primary nephrotic syndrome (PNS) [4][5][6][7][8].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

The role of adiponectin and its receptor in patients with idiopathic membranous nephropathy complicated with hyperuricemia

et al. 2021

View full text Add to dashboard Cite

Introduction/Objective. This study aimed to assess the changes of adiponectin (APN), IL-1?, adiponectin receptor 1 (Adipo R1), and NLRP3 expression of patients with idiopathic membranous nephropathy (IMN) complicated with hyperuricemia (HUA) and analyze the relationship between the APN pathway and the NLRP3 pathway. Methods. Forty-eight patients with IMN+HUA group, 49 patients with IMN group, 30 healthy controls, and 24 samples of healthy renal tissue were evaluated. APN and IL-1? of each group were detected by the ELISA method. AdipoR1 and NLRP3 in kidney tissue were detected by immunohistochemistry. The clinical data of each group were collected, and the relationship between APN, IL-1?, AdipoR1, NLRP3, and other indexes was analyzed. Results. (1) The concentration of UA, APN, IL-1?, and NLRP3 in the IMN+HUA group are significantly higher than those in the IMN group, but the AdipoR1 was lower. (2) With the severity of CKD stage, APN, IL-1?, and NLRP3 gradually increased in IMN+HUA group, but AdipoR1 gradually decreased. However, the above indicators did not change significantly in the IMN stages. Conclusion. The AdipoR1-AMPK and NLRP3-caspase-1-IL-1? signaling pathway may play an essential role in IMN+HUA patients. The intervention of these two pathways may make a great significance to the occurrence and progression on IMN+HUA patients.

show abstract

Section: Discussionmentioning

confidence: 60%

Section: Introductionmentioning

confidence: 99%

The role of adiponectin and its receptor in patients with idiopathic membranous nephropathy complicated with hyperuricemia

et al. 2021

View full text Add to dashboard Cite

show abstract

“…CKD is becoming a public health problem, which affects more than 10% of the global population (Huang et al., 2021 ). Although initiated by various aetiologies, renal fibrosis is a final common pathological change in all types of CKD (Gewin, 2018 ; Jing et al., 2020 ). Although therapies such as dialysis and transplantation can ameliorate or delay the progression of renal fibrosis, there are currently no curative strategies (Nastase et al., 2018 ).…”

Section: Discussionmentioning

confidence: 99%

β‐catenin‐controlled tubular cell‐derived exosomes play a key role in fibroblast activation via the OPN‐CD44 axis

Chen

Zhang

et al. 2022

J of Extracellular Vesicle

View full text Add to dashboard Cite

Tubular injury and peripheral fibroblast activation are the hallmarks of chronic kidney disease (CKD), suggesting intimate communication between the two types of cells. However, the underlying mechanisms remain to be determined. Exosomes play a role in shuttling proteins and other materials to recipient cells. In our study, we found that exosomes were aroused by β‐catenin in renal tubular cells. Osteopontin (OPN), especially its N‐terminal fragment (N‐OPN), was encapsulated in β‐catenin‐controlled tubular cell‐derived exosome cargo, and subsequently passed to fibroblasts. Through binding with CD44, exosomal OPN promoted fibroblast proliferation and activation. Gene deletion of β‐catenin in tubular cells (Ksp‐β‐catenin −/− ) or gene ablation of CD44 (CD44 −/− ) greatly ameliorated renal fibrosis. Notably, N‐OPN was carried by exosome and secreted into the urine of patients with CKD, and negatively correlated with kidney function. The urinary exosomes from patients with CKD greatly accelerated renal fibrosis, which was blocked by CD44 deletion. These results suggest that exosome‐mediated activation of the OPN/CD44 axis plays a key role in renal fibrosis, which is controlled by β‐catenin.

show abstract

“…The high morbidity and mortality of CKD brings a heavy burden to medical care and economy development ( Jha et al, 2012 ; Nastase et al, 2018 ). Notably, renal fibrosis is the key pathological feature in the progression of CKD into ESRD ( Gewin, 2018 ; Jing et al, 2020 ). To clarify the underlying mechanisms of renal fibrosis is valuable to retard the development of CKD and lessens the medical and financial burden.…”

Section: Introductionmentioning

confidence: 99%

CXC Chemokine Receptor 2 Accelerates Tubular Cell Senescence and Renal Fibrosis via β-Catenin-Induced Mitochondrial Dysfunction

Meng

Huang

Ling

et al. 2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Renal fibrosis is a common feature of various chronic kidney diseases (CKD). However, its underlying mechanism has not been totally clarified. C-X-C motif chemokine receptor (CXCR) family plays a role in renal fibrosis, however, detailed mechanisms have not been elucidated. Here, we report that CXCR2 has a potential role in tubular cell senescence and renal fibrosis, and is associated with β-catenin-activated mitochondrial dysfunction. CXCR2 is one of most increased members among CXCR family in unilateral ureteral obstruction (UUO) mice. CXCR2 was expressed primarily in tubules and co-localized with p16INK4A, a cellular senescence marker, and β-catenin. Administration of SB225002, a selective CXCR2 antagonist, significantly inhibited the activation of β-catenin signaling, restored mitochondrial function, protected against tubular cell senescence and renal fibrosis in unilateral ureteral obstruction (UUO) mice. In unilateral ischemia-reperfusion injury (UIRI) mice, treatment with interlukin-8 (IL-8), the ligand of CXCR2, further aggravated β-catenin activation, mitochondrial dysfunction, tubular cell senescence and renal fibrosis, whereas knockdown of p16INK4A inhibited IL-8-induced these effects. In vitro, SB225002 inhibited mitochondrial dysfunction and tubular cell senescence. Furthermore, ICG-001, a β-catenin signaling blocker, significantly retarded CXCR2-induced cellular senescence and fibrotic changes. These results suggest that CXCR2 promotes tubular cell senescence and renal fibrosis through inducing β-catenin-activated mitochondrial dysfunction.

show abstract

Adiponectin in renal fibrosis

Cited by 24 publications

References 83 publications

The role of adiponectin and its receptor in patients with idiopathic membranous nephropathy complicated with hyperuricemia

The role of adiponectin and its receptor in patients with idiopathic membranous nephropathy complicated with hyperuricemia

β‐catenin‐controlled tubular cell‐derived exosomes play a key role in fibroblast activation via the OPN‐CD44 axis

CXC Chemokine Receptor 2 Accelerates Tubular Cell Senescence and Renal Fibrosis via β-Catenin-Induced Mitochondrial Dysfunction

Contact Info

Product

Resources

About