Evidence map›Paper›PMID 39910210›Full record

ReviewActa pharmacologica Sinica2025

Cardiorenal syndrome: clinical diagnosis, molecular mechanisms and therapeutic strategies.

Bo-Rui Zhao, Xin-Rong Hu, Wei-Dong Wang, Yi Zhou

Abstract readReview
In one paragraph

Review in Acta pharmacologica Sinica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing 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

55 citing papers in PubMed.

  1. The efficacy ofRenal failure · 2026
    Article
  2. Review
  3. Herbacetin as a novel therapeutic agent for pulmonary and renal fibrosis by targeting TGFBR2 for degradation.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Gastrodin as a nephroprotective agent: Molecular docking-based modulation of oxidative stress, fibrosis, and inflammation.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026
    Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
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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

4 authors.

Bo-Rui Zhao *Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Xin-Rong Hu *Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China.
Wei-Dong WangInstitute of Hypertension, Zhongshan School of Medicine, Sun Yat-sen University, Guangzhou, 510080, China.
Yi ZhouDepartment of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, 510080, China. zhouyi39@mail.sysu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

As the heart and kidneys are closely connected by the circulatory system, primary dysfunction of either organ usually leads to secondary dysfunction or damage to the other organ. These interactions play a major role in the pathogenesis of a clinical entity named cardiorenal syndrome (CRS). The pathophysiology of CRS is complicated and involves multiple body systems. In early studies, CRS was classified into five subtypes according to the organs associated with the vicious cycle and the acuteness and chronicity of CRS. Increasing evidence shows that CRS is associated with a variety of pathological mechanisms, such as haemodynamics, neurohormonal changes, hypervolemia, hypertension, hyperuraemia and hyperuricaemia. In this review, we summarize the classification and currently available diagnostic biomarkers of CRS. We highlight the recently revealed molecular pathogenesis of CRS, such as oxidative stress and inflammation, hyperactive renin‒angiotensin‒aldosterone system, maladaptive Wnt/β-catenin signalling pathway and profibrotic TGF‒β1/Smad signalling pathway, as well as other pathogeneses, such as dysbiosis of the gut microbiota and dysregulation of noncoding RNAs. Targeting these CRS-associated signalling pathways has new therapeutic potential for treating CRS. In addition, various chemical drugs, natural products, complementary therapies, blockers, and agonists that protect against CRS are summarized. Since the molecular mechanisms of CRS remain to be elucidated, no single intervention has been shown to be effective in treating CRS. Pharmacologic therapies designed to block CRS are urgently needed. This review presents a critical therapeutic avenue for targeting CRS and concurrently illuminates challenges and opportunities for discovering novel treatment strategies for CRS.

Indexed as

Cardio-Renal SyndromeAnimalsBiomarkersHumansOxidative StressSignal TransductionBiomarkerscardiorenal syndromegut microbiotanoncoding RNAsoxidative stress and inflammationrenin–angiotensin–aldosterone systemTGF-β1/Smad

Identifiers

PMID39910210
PMCPMC12098865

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.