Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damage

20 May 2025

Abstract excerpt

DNA repair is essential for preserving genome integrity. Podocytes, postmitotic epithelial cells of the kidney filtration unit, bear limited regenerative capacity, yet their survival is indispensable for kidney health. Podocyte loss is a hallmark of the aging process and of many diseases, but the underlying factors remain unclear. We investigated the consequences of DNA damage in a podocyte-specific knockout...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Genetic and Kidney Cyst Diseases
Share to Renal Diseases and Glomerulopathies

Source

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Identifiers

PMID: 40392611
DOI: 10.1172/jci.insight.172370

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damagePMID 40392611Read ↗

Loss of genome maintenance accelerates podocyte damage and agingSemantic proximity Read ↗

Podocyte-specific RAP1GAP expression contributes to focal segmental glomerulosclerosis–associated glomerular injurySemantic proximity Read ↗

Modeling injury and repair in kidney organoids reveals that homologous recombination governs tubular intrinsic repairSemantic proximity Read ↗

Profilin1 is required for prevention of mitotic catastrophe in murine and human glomerular diseasesSemantic proximity Read ↗

A single cell atlas of mouse podocytes upon injury identifies kidney zone-dependent responsesSemantic proximity Read ↗

Role of mTOR in podocyte function and diabetic nephropathy in humans and mice.Semantic proximity Read ↗

Epigenetic Alterations in Podocytes in Diabetic NephropathySemantic proximity Read ↗

p53 regulates diverse tissue-specific outcomes to endogenous DNA damage in miceSemantic proximity Read ↗

DNA damage in proximal tubules triggers systemic metabolic dysfunction through epigenetically altered macrophagesSemantic proximity Read ↗

Cell Cycle Regulatory Proteins in Podocyte Health and DiseaseSemantic proximity Read ↗

Epigenetic transcriptional reprogramming by WT1 mediates a repair response during podocyte injurySemantic proximity Read ↗

Persistent DNA damage underlies tubular cell polyploidization and progression to chronic kidney disease in kidneys deficient in the DNA repair protein FAN1Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.