ReviewInternational journal of molecular sciences2026
Chronic Kidney Disease and Cellular Senescence.
Review in International journal of molecular sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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.
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.
Who cites it
4 citing papers in PubMed.
- Uremic Serum Alters Gene Expression Profiles and Signaling Pathway Activity in Porcine Arterial Smooth Muscle Cells.Biomolecules · 2026Article
- Mechanisms of Obesity-Related Kidney Disease: From Adipose Depot Biology to the Chymase-Aldosterone and Ghrelin-Leptin Axes.Biomolecules · 2026Review
- Cellular senescence and inflammageing: from mechanisms to senotherapeutic interventions.Biogerontology · 2026Review
- Cellular senescence in kidney diseases: a bibliometric analysis of global trends, knowledge bases, and emerging therapeutic frontiers.International urology and nephrology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Chronic kidney disease (CKD) and kidney aging share many pathological and molecular features, with cellular senescence emerging as a potentially important contributor to disease progression. Senescent cells accumulate in the kidneys due to persistent stressors, contributing to chronic inflammation and fibrosis via the senescence-associated secretory phenotype (SASP). This review explores the intersection between CKD and renal aging, focusing on the mechanisms driving senescence, its impact on kidney function, and potential therapeutic interventions. We explore various senotherapeutic approaches, such as senolytics, senomorphics, and rejuvenating agents, and highlight the increasing role of artificial intelligence (AI) and machine learning (ML) in detecting and monitoring senescent cells, enabling high-throughput and precise assessment across experimental and clinical settings. Understanding these mechanisms offers new avenues for developing targeted treatments to slow CKD progression and improve patient outcomes.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.