ReviewInternational journal of molecular medicine2025
Role of the TGF‑β/Smad signaling pathway in the transition from acute kidney injury to chronic kidney disease (Review).
Review in International journal of molecular medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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.
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Who cites it
5 citing papers in PubMed.
- Transition from acute kidney injury to chronic kidney disease: molecular mechanisms and therapeutic interventions.Molecular biomedicine · 2026Review
- Network Pharmacology and Molecular Docking-Based Investigation of Empagliflozin's Therapeutic Potential in Chronic Kidney Disease.Life (Basel, Switzerland) · 2026Article
- The core mechanism of hypertension-linked renal fibrosis: "RAAS-ROS-inflammation-fibrosis" axis.iScience · 2026Review
- Spatiotemporal Control of Intercellular Crosstalk: A New Therapeutic Paradigm for Halting Acute Kidney Injury to Chronic Kidney Disease Transition.Biomolecules · 2026Review
- The Function of the TGFβ Signaling Pathway in Connective Tissue Diseases: From Biology to Clinical Application.Journal of inflammation research · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The progression from acute kidney injury (AKI) to chronic kidney disease (CKD) has become a focal point of investigation, with the TGF‑β/Smad signaling pathway emerging as a key mediator in this process. The present review assesses how TGF‑β/Smad contributes to renal fibrosis and the subsequent deterioration of kidney function following AKI. Drawing on recent experimental and clinical findings, this study explores how pathway activation promotes tubular cell injury, inflammation and interstitial fibrosis. By examining these molecular and cellular events, this study offers fresh insights into the complex mechanisms that underlie the AKI‑CKD transition and highlights potential therapeutic strategies aimed at interrupting or slowing disease progression.
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Registered trials
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.