Evidence map›Paper›PMID 38601984›Full record

ReviewAmerican journal of physiology. Renal physiology2024

Mechanisms and implications of podocyte autophagy in chronic kidney disease.

Rachel Njeim, Sandra Merscher, Alessia Fornoni

Abstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed.

  1. Review
  2. Article
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  10. Review
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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

3 authors.

Rachel NjeimKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, United States.
Sandra MerscherKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, United States.ORCID 0000-0002-4757-7494
Alessia FornoniKatz Family Division of Nephrology and Hypertension, Department of Medicine, University of Miami Miller School of Medicine, Miami, Florida, United States.ORCID 0000-0002-1313-7773

Funding

Training Program in Clinical & Translationa Research in Human Glomerular DiseaseU54DK083912 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI HOLZMAN, LAWRENCE B. · 2009 to 2023
$20.3M
Miami Clinical and Translational Science InstituteUM1TR004556 · NCATS · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Olveen Carrasquillo, ERIN N KOBETZ · 2023 to 2026
$16.0M
CureGN-Penn PCCU01DK100846 · NIDDK · UNIVERSITY OF PENNSYLVANIA · PI LAWRENCE B. HOLZMAN · 2019 to 2026
$8.3M
1/13 ApoL1 Genotypes in Kidney Donors and Long-Term Outcomes in Kidney Transplant Recipients Clinical CenterU01DK116101 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ALESSIA FORNONI, Mariella Cecilia Ortigosa-goggins · 2017 to 2026
$2.4M
APOM deficiency contributes to renal failure in glomerular diseasesR01DK136679 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI ALESSIA FORNONI · 2023 to 2026
$1.9M
Workshops and Coaching to Foster Career Skills in Newly Funded NIDDK ScholarsUE5DK137308 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI Ashutosh Agarwal, ALESSIA FORNONI · 2023 to 2026
$648k
Crosstalk between lipid droplets and other organelles in podocytesR56DK104753 · NIDDK · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI FORNONI, ALESSIA · 2023 to 2023
$100k
Aurinia PharmaceuticsHHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R01DK136679HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R56DK104753NCATS NIH HHS UM1 TR004556NIDDK NIH HHS R01 DK136679NIDDK NIH HHS R56 DK104753NIDDK NIH HHS U01 DK100846NIDDK NIH HHS U01 DK116101NIDDK NIH HHS U54 DK083912NIDDK NIH HHS UE5 DK137308Pfizer (Davis)UM | Miami Clinical and Translational Science Institute, University of Miami (CTSI) U01DK100846UM | Miami Clinical and Translational Science Institute, University of Miami (CTSI) U01DK116101UM | Miami Clinical and Translational Science Institute, University of Miami (CTSI) U54DK083912UM | Miami Clinical and Translational Science Institute, University of Miami (CTSI) UE5DK137308UM | Miami Clinical and Translational Science Institute, University of Miami (CTSI) UM1TR004556
6 · The paper itself

Abstract

Autophagy is a protective mechanism through which cells degrade and recycle proteins and organelles to maintain cellular homeostasis and integrity. An accumulating body of evidence underscores the significant impact of dysregulated autophagy on podocyte injury in chronic kidney disease (CKD). In this review, we provide a comprehensive overview of the diverse types of autophagy and their regulation in cellular homeostasis, with a specific emphasis on podocytes. Furthermore, we discuss recent findings that focus on the functional role of different types of autophagy during podocyte injury in chronic kidney disease. The intricate interplay between different types of autophagy and podocyte health requires further research, which is critical for understanding the pathogenesis of CKD and developing targeted therapeutic interventions.

Indexed as

AutophagyPodocytesRenal Insufficiency, ChronicAnimalsHomeostasisHumansSignal Transductionautophagychronic kidney diseasepodocyte injury

Identifiers

PMID38601984
PMCPMC11386983

What OpenQuestion holds

Textmetadata
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.