Poricoic acid A attenuates renal fibrosis by inhibiting endoplasmic reticulum stress-mediated apoptosis DOI Creative Commons
Hui Zhao, Tian Liu, Chang-E Yang

et al.

Brazilian Journal of Medical and Biological Research, Journal Year: 2024, Volume and Issue: 57

Published: Jan. 1, 2024

Renal fibrosis is a common manifestation in the progression of chronic kidney disease (CKD) to failure. Currently, there no available therapy prevent renal fibrosis. Poricoic acid A (PAA) isolated from Poria cocos shows notable antifibrotic effects. However, its potential mechanism still unclear. This study aimed evaluate effects and mechanisms PAA against mouse model was established using unilateral ureteral obstruction (UUO). We showed that administration significantly alleviated lesions collagen deposition UUO mice. Mice with resulted epithelial-to-mesenchymal transition (EMT) activation endoplasmic reticulum stress (ERS) tissues, while treatment inhibited EMT ERS activation. Additionally, markedly ERS-mediated apoptosis Molecular docking results indicated stably combined GRP78 ATF4. In conclusion, these demonstrated possesses significant bioactivity might be inhibition apoptosis.

Language: Английский

Protective effect of compound K against podocyte injury in chronic kidney disease by maintaining mitochondrial homeostasis DOI Creative Commons

Fugang Huang,

Shuo Huang, Ke Sun

et al.

Scientific Reports, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 2, 2025

Chronic kidney disease (CKD) stands as a formidable global health challenge, often advancing to end-stage renal (ESRD) with devastating morbidity and mortality. At the central of this progression lies podocyte injury, critical determinant glomerular dysfunction. Compound K (CK), bioactive metabolite derived from ginsenoside, has emerged compelling candidate for nephroprotective therapy. Here, we unveil profound therapeutic potential CK in folic acid (FA)-induced CKD mouse model, demonstrating its ability restore function mitigate injury. exerted effects by reinforcing inter-podocyte junctions, suppressing aberrant motility, preventing detachment apoptosis, thereby safeguarding filtration barrier. Mechanistically, identified mitochondrial dysregulation key driver excessive oxidative stress, which is commonly associated damage. remarkably restored homeostasis attenuating pathological fission enhancing mitophagy, rebalancing delicate network. Intriguingly, may disrupt formation Drp1-Bax dimer, crucial mediator further averting loss. Collectively, our findings highlight potent agent, offering novel avenue management redefining possibilities battle against progressive disease.

Language: Английский

Citations

2

The role of mitophagy in metabolic diseases and its exercise intervention DOI Creative Commons

Shaokai Tang,

Yuanwen Geng,

Qinqin Lin

et al.

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

Published: Jan. 29, 2024

Mitochondria are energy factories that sustain life activities in the body, and their dysfunction can cause various metabolic diseases threaten human health. Mitophagy, an essential intracellular mitochondrial quality control mechanism, maintain cellular homeostasis by removing damaged mitochondria participating developing diseases. Research has confirmed exercise regulate mitophagy levels, thereby exerting protective effects This article reviews role of diseases, on mitophagy, potential mechanisms exercise-regulated intervention providing new insights for future basic clinical research interventions to prevent treat

Language: Английский

Citations

9

Poria cocos: traditional uses, triterpenoid components and their renoprotective pharmacology DOI

Zhi-yuan Guo,

X. Wu,

Shui-juan Zhang

et al.

Acta Pharmacologica Sinica, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 31, 2024

Language: Английский

Citations

8

Bibliometric analysis of literature on natural medicines against chronic kidney disease from 2001 to 2024 DOI
Xiaoqing Shi, Hongmei Yin, Xiaodan Shi

et al.

Phytomedicine, Journal Year: 2025, Volume and Issue: unknown, P. 156410 - 156410

Published: Jan. 1, 2025

Language: Английский

Citations

0

Poricoic Acid A Protects Against High-Salt-Diet Induced Renal Fibrosis by Modulating Gut Microbiota and SCFA Metabolism DOI
Xiaoyue Wang,

Xu Yi,

Yonghua Wang

et al.

Plant Foods for Human Nutrition, Journal Year: 2025, Volume and Issue: 80(2)

Published: April 29, 2025

Language: Английский

Citations

0

Progress in the study of bioactivity, chemical composition and pharmacological mechanism of action in Wolfiporia cocos (F.A. Wolf) Ryvarden & Gilb DOI Creative Commons
Qi Xiong, Zhuoran Li,

Defeng Yang

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: March 3, 2025

The Latin name of Wolfiporia cocos is (F.A. Wolf) Ryvarden & Gilb, it a medicinal and edible mushroom belonging to the family Polyporaceae. Traditional Chinese medicine believes that can strengthen spleen, diuretic, tranquillise mind dispel dampness. So far, chemical active metabolites isolated extracted from are mainly polysaccharides, triterpenoids, sterols. Modern pharmacology has found these have wide range pharmacological effects, including antitumour, antioxidation, anti-inflammatory, immunomodulation, regulation intestinal flora, glycolipid metabolism, improvement organ function. By applying Poria , cocos, Gilb as search terms, we searched all relevant studies on Web Science PubMed databases classified categories according main research content each literature summarized its mechanism action, updated latest results, discussed direction further in future provide better reference for clinical applications with therapeutic effects potential value.

Language: Английский

Citations

0

Important regulatory role of mitophagy in diabetic microvascular complications DOI Creative Commons
Xiaohan Hu, Jiao Lv, Yunyun Zhao

et al.

Journal of Translational Medicine, Journal Year: 2025, Volume and Issue: 23(1)

Published: March 4, 2025

Microvascular complications of diabetes pose a significant threat to global health, mainly including diabetic kidney disease (DKD), retinopathy (DR), peripheral neuropathy (DPN), and cardiomyopathy (DCM), which can ultimately lead failure, blindness, disability, heart failure. With the increasing prevalence diabetes, search for new therapeutic targets microvascular is imminent. Mitophagy widespread strictly maintained process self-renewal energy metabolism that plays an important role in reducing inflammatory responses, inhibiting reactive oxygen species accumulation, maintaining cellular metabolism. Hyperglycemia results impaired mitophagy, leads mitochondrial dysfunction exacerbates progression. This article summarizes relevant molecular mechanisms mitophagy reviews current status research on regulating as potential treatment complications, attempting give angles complications.

Language: Английский

Citations

0

Multiple roles of mitochondrial autophagy receptor FUNDC1 in mitochondrial events and kidney disease DOI Creative Commons
Kaiqing Li, Xue Xia, Ying Tong

et al.

Frontiers in Cell and Developmental Biology, Journal Year: 2024, Volume and Issue: 12

Published: Oct. 9, 2024

This article reviews the latest research progress on role of mitochondrial autophagy receptor FUN14 domain containing 1 (FUNDC1) in events and kidney disease. FUNDC1 is a protein located outer membrane mitochondria, which maintains function quality mitochondria by regulating autophagy, that is, selective degradation process mitochondria. The structural characteristics enable it to respond intracellular signal changes regulate activity through phosphorylation dephosphorylation. During phosphorylation, unc-51-like kinase (ULK1) promotes activation mitophagy phosphorylating Ser17 FUNDC1. In contrast, Src CK2 kinases inhibit interaction between LC3 Tyr18 Ser13, thereby inhibiting mitophagy. dephosphorylation, PGAM5 phosphatase enhances dephosphorylating activating BCL2L1 inhibits interacting with PGAM5, preventing dephosphorylation plays an important events, participating fission, maintaining homeostasis iron proteins matrix, mediating crosstalk endoplasmic reticulum lysosomes, have effects cell energy metabolism programmed death. aspect disease, abnormal closely related occurrence development many diseases. acute injury (AKI), cardiorenal syndrome (CRS), diabetic nephropathy (DN), chronic disease (CKD) ,renal fibrosis (RF) renal anemia, FUNDC1-mediated imbalance may be one key factors progression. Therefore, in-depth study regulatory mechanism great significance for understanding pathogenesis developing new treatment strategies.

Language: Английский

Citations

3

Poricoic acid a ameliorates high glucose-induced podocyte injury by regulating the AMPKα/FUNDC1 pathway DOI
Yuwen Wu, Yancheng Xu,

Haohua Deng

et al.

Molecular Biology Reports, Journal Year: 2024, Volume and Issue: 51(1)

Published: Sept. 21, 2024

Language: Английский

Citations

1

Poricoic acid A promotes angiogenesis and myocardial regeneration by inducing autophagy in myocardial infarction DOI
Jin Qu,

Jinzhu Yin,

Zhaozheng Liu

et al.

Tissue and Cell, Journal Year: 2024, Volume and Issue: 88, P. 102401 - 102401

Published: May 3, 2024

Language: Английский

Citations

1