Novel Drug Candidates for the Treatment of Cardiac and Renal Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 30 June 2026 | Viewed by 1377

Special Issue Editors


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Guest Editor
Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, Mexico City 04510, Mexico
Interests: mitochondrial dysfunction; inflammation; bioenergetics, cardiac diseases; renal diseases; treatments; antioxidants

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Guest Editor
Departamento de Farmacología, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de Mexico 04510, Mexico
Interests: renal diseases; diabetes; metabolic syndrome; oxidative stress; antioxidants
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Special Issue Information

Dear Colleagues,

Kidney diseases are a growing health problem worldwide that can lead to the development of cardiac alterations, causing millions of deaths. Renal and cardiac diseases are intrinsically related through the pathology known as cardiorenal syndrome (CRS), which consists of acute or chronic failure of the kidney or heart that leads to dysfunction of the other organ. Thus, five subtypes of CRS are highly prevalent due to the global prevalence of heart and renal pathologies. Recent research has advanced our understanding of CRS, and factors such as redox alterations, oxidative stress, inflammation, dyslipidemia and fibrosis are recognized as potential triggers of this pathology. However, specific therapies are not yet available for clinical routine.

Therefore, we welcome submissions to our Special Issue entitled “Novel Drug Candidates for the Treatment of Cardiac and Renal Diseases”. Manuscripts focusing on novel treatments for renal and/or cardiac diseases are welcome to further advance our understanding in this area.

Dr. Ana Karina Aranda-Rivera
Prof. Dr. José Pedraza Chaverri
Dr. Diana Barrera-Oviedo
Guest Editors

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Keywords

  • kidney diseases
  • cardiac diseases
  • cardiorenal syndrome
  • treatments
  • chronic kidney diseases
  • drugs
  • dyslipidemia
  • oxidative stress

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Published Papers (1 paper)

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Research

18 pages, 3879 KB  
Article
7-Ketolithocholic Acid Exerts Anti-Renal Fibrotic Effects Through FXR-Mediated Inhibition of TGF-β/Smad and Wnt/β-Catenin Pathways
by Qicheng Guo, Lianye Peng, Jingyi Zhang, Junming Hu, Yinyin Wang, Jiali Wei and Zhihao Zhang
Pharmaceuticals 2026, 19(1), 15; https://doi.org/10.3390/ph19010015 - 21 Dec 2025
Cited by 1 | Viewed by 802
Abstract
Background/Objectives: To explore the protective effects of 7-Ketolithocholic acid (7-KLCA) against renal fibrosis and its mechanism, focusing on its interaction with farnesoid X receptor (FXR). Methods: In vitro, TGF-β-induced fibrosis in HK-2/NRK-49F cells and LPS-induced inflammation in HK-2 cells were detected by CCK-8, [...] Read more.
Background/Objectives: To explore the protective effects of 7-Ketolithocholic acid (7-KLCA) against renal fibrosis and its mechanism, focusing on its interaction with farnesoid X receptor (FXR). Methods: In vitro, TGF-β-induced fibrosis in HK-2/NRK-49F cells and LPS-induced inflammation in HK-2 cells were detected by CCK-8, Western blot, and qPCR. In vivo, unilateral ureteral obstruction (UUO) and adenine (Ade)-induced mouse models were treated with a low/high-dose 7-KLCA or losartan. Renal injury was evaluated via H&E/Masson staining, serum creatinine (SCR), and blood urea nitrogen (BUN) levels. The 7-KLCA-FXR interaction was verified by molecular docking, CETSA, and DARTS. FXR downstream genes and related proteins were measured by WB and qPCR. Results: 7-KLCA inhibited the expression of fibrotic proteins (fibronectin, collagen-I) and reduced the LPS-induced release of inflammatory factors (IL-1β, IL-6). In mice, it alleviated renal swelling, collagen deposition, and tubular damage, while lowering serum SCR and BUN levels. Mechanistically, 7-KLCA stably bound to the FXR ligand-binding domain, enhanced its thermal stability and degradation resistance. It upregulated FXR and its downstream genes SHP and FGF15, thereby inhibiting the activation of TGF-β/Smad and Wnt/β-catenin pathways. Conclusions: This is the first study to clarify the molecular mechanism through which 7-KLCA targets FXR and dually suppresses the key pro-fibrotic pathways TGF-β/Smad and Wnt/β-catenin, thereby exerting anti-renal fibrosis effects. Full article
(This article belongs to the Special Issue Novel Drug Candidates for the Treatment of Cardiac and Renal Diseases)
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