Evidence map›Paper›PMID 33562139›Full record

ArticleInternational journal of molecular sciences2021

Geniposide Improves Diabetic Nephropathy by Enhancing ULK1-Mediated Autophagy and Reducing Oxidative Stress through AMPK Activation.

Theodomir Dusabimana, Eun Jung Park, Jihyun Je, Kyuho Jeong, Seung Pil Yun, Hye Jung Kim, Hwajin Kim, Sang Won Park

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
8.5field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Theodomir DusabimanaDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.ORCID 0000-0002-8337-4969
Eun Jung ParkDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.
Jihyun JeDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.
Kyuho JeongDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.
Seung Pil YunDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.
Hye Jung KimDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.ORCID 0000-0002-7067-6810
Hwajin KimDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.ORCID 0000-0002-7181-3696
Sang Won ParkDepartment of Pharmacology, Institute of Health Sciences, Gyeongsang National University College of Medicine, Jinju 52727, Korea.ORCID 0000-0002-6149-5284
Gyeongsang National University · KR

Funding

National Research Foundation of Korea NRF-2015R1A5A2008833National Research Foundation of Korea NRF-2017R1A2B4009387
6 · The paper itself

Abstract

Diabetic nephropathy (DN) is a common pathological feature in patients with diabetes and the leading cause of end-stage renal disease. Although several pharmacological agents have been developed, the management of DN remains challenging. Geniposide, a natural compound has been reported for anti-inflammatory and anti-diabetic effects; however, its role in DN remains poorly understood. This study investigated the protective effects of geniposide on DN and its underlying mechanisms. We used a C57BL/6 mouse model of DN in combination with a high-fat diet and streptozotocin after unilateral nephrectomy and treated with geniposide by oral gavage for 5 weeks. Geniposide effectively improves DN-induced renal structural and functional abnormalities by reducing albuminuria, podocyte loss, glomerular and tubular injury, renal inflammation and interstitial fibrosis. These changes induced by geniposide were associated with an increase of AMPK activity to enhance ULK1-mediated autophagy response and a decrease of AKT activity to block oxidative stress, inflammation and fibrosis in diabetic kidney. In addition, geniposide increased the activities of PKA and GSK3β, possibly modulating AMPK and AKT pathways, efficiently improving renal dysfunction and ameliorating the progression of DN. Conclusively, geniposide enhances ULK1-mediated autophagy and reduces oxidative stress, inflammation and fibrosis, suggesting geniposide as a promising treatment for DN.

Indexed as

AMP-Activated Protein KinasesAnimalsAnti-Inflammatory AgentsAutophagyAutophagy-Related Protein-1 HomologCyclic AMP-Dependent Protein KinasesDiabetes ComplicationsDiabetes Mellitus, ExperimentalDiabetic NephropathiesDiet, High-FatDisease Models, AnimalFibrosisGlycogen Synthase Kinase 3 betaIridoidsMiceMice, Inbred C57BLAMP-Activated Protein KinasesAnti-Inflammatory AgentsAutophagy-Related Protein-1 HomologCyclic AMP-Dependent Protein KinasesgeniposideGlycogen Synthase Kinase 3 betaIridoidsUlk1 protein, mouseAMPKautophagydiabetic nephropathygeniposideinflammationoxidative stress

Identifiers

PMID33562139
PMCPMC7915505
OpenAlexW3126635562

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.