Evidence map›Paper›PMID 41904121›Full record

ArticleCell death discovery2026

AMPK is dispensable for physiological podocyte and glomerular functions but prevents glomerular fibrosis in experimental diabetes.

Swayam Prakash Srivastava, Olivia Kopasz-Gemmen, Abhiram Kunamneni, Aaron Thurman, Shota Yoshida, Eden Ozkan, Vinamra Swaroop, Rahul Nanwani, Ajan Arora, Arya Joshi and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

20 authors.

Swayam Prakash SrivastavaLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA. spsr@umich.edu.ORCID http://orcid.org/0000-0002-7162-3091
Olivia Kopasz-GemmenLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Abhiram KunamneniLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Aaron ThurmanLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Shota YoshidaLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Eden OzkanLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Vinamra SwaroopLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Rahul NanwaniLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Ajan AroraLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Arya JoshiLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Om KhuperkarLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Mariam HamedLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Mihir Suresh BharadwajLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Niloy IslamLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Adesh UrvalLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Junying WangLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Sungki HongLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA.
Keizo KanasakiDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Japan.
Daisuke KoyaDepartment of Diabetology and Endocrinology, Kanazawa Medical University, Uchinada, Japan.
Ken InokiLife Sciences Institute, University of Michigan, Ann Arbor, MI, USA. inokik@umich.edu.ORCID http://orcid.org/0000-0001-8882-444X

Funding

Lysosomal cholesterol-dependent anabolic regulationR01DK124709 · UNIVERSITY OF MICHIGAN AT ANN ARBOR · 2025 to 2025
$522k
NIDDK NIH HHS R01 DK124709NIGMS NIH HHS R01 GM110019
6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) has been postulated to be crucial in regulating various renal physiology and pathophysiology processes, including energy metabolism, ion and water transport, inflammation, and hypertrophy. However, the specific roles of AMPK in podocytes, cells critical for maintaining glomerular filtration, have not been fully explored using genetic model animals. In this study, we generated mice lacking both AMPK α1 and α2 catalytic subunits in glomerular podocytes (pmut). Our findings revealed that, surprisingly, AMPK is dispensable for normal podocyte function. These knockout mice could live as long as their wild-type littermates without showing any pathological alterations in their glomeruli or glomerular function at two years of age. However, under diabetic conditions, the diabetic pmut mice exhibited increased lipid and collagen accumulation and an elevated expression of mesenchymal proteins in their glomeruli. They also showed more significant albuminuria compared to control diabetic mice. Under high-glucose culture conditions, glomeruli isolated from pmut mice showed reduced expression of mitochondrial genes (e.g., Ndufv2) and increased leakage of mitochondrial components. Additionally, there was increased expression of genes associated with nucleotide-sensing and pro-inflammatory pathways (including mb21d2, IL-1β, and NF-κB). These observations suggest that while AMPK is not necessary for podocyte function in healthy kidneys, it is crucial for preventing glomerular fibrosis resulting from lipotoxicity and inflammation under diabetic conditions.

Identifiers

PMID41904121
PMCPMC13153347

What Socratic holds

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Registered trials

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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 Socratic graph.