IJRR

International Journal of Research and Review

| Home | Current Issue | Archive | Instructions to Authors | Journals |

Year: 2026 | Month: August | Volume: 13 | Issue: 8 | Pages: 328-351

DOI: https://doi.org/10.52403/ijrr.20260832

Role of TGF-beta1/Smad/CCL2 Axis in High-Glucose Dialysis-Induced Peritoneal Fibrosis: A PRISMA 2020-Compliant Quantitative Systematic Review

Bade Mohamed Abdi1, Dafeng He2, Abdalla Mohamed3

1,2Department of Nephrology, 3Department of Gastroenterology,
Northern Jiangsu People's Hospital, Yangzhou City, Jiangsu, China.

Corresponding Author: Dafeng He

ABSTRACT

Background: Peritoneal dialysis (PD) is a treatment which leaves the mesothelial and immune cells in contact with hyperosmolar, glucose-rich dialysate. Mesothelial-mesenchymal transition, inflammatory mechanisms, angiogenic mechanisms, oxidative/metabolic stress and TGF-beta/Smad signalling have all been reported to be central mechanisms in peritoneal fibrosis in recent reviews.
Objective: To compile the quantitative evidence produced in 2019-2026 which is verified as objective and quantitative evidence of TGF-beta1/Smad/CCL2 axis and related mechanisms of high glucose dialysis-induced peritoneal fibrosis, focusing on statistics, study design and risk of bias.
Methods: A protocol for conducting the PRISMA 2020 was followed and predefined PICOS were used, search strings were used exactly as written, duplicate screening, retraction/expression-of-concern checks, data extraction at the level of study and risk-of-bias appraisal were performed. PRISMA 2020 reporting standard was followed.
Results: 42 confirmed primary studies were retained. The largest publication cluster was 2022 (10/42, 23.8%), followed by 2021 and 2023 (7/42 each, 16.7% each). Overall, ~50% of included records included direct measure or intervention in TGF-beta/Smad, while the measure of CCL2/MCP-1 was seen in fewer studies, primarily in SGLT2/high glucose induced mesothelial and inflammation models.
Conclusions: There is evidence for a mechanistic hierarchy with high glucose PD exposure inducing metabolic and inflammatory stressors that all converge on TGF-beta/Smad signalling. Because the CCL2/MCP-1 arm is a biologically plausible but under-quantified pathway compared to TGF-beta/Smad, it is important to note that the complete TGF-beta1/Smad/CCL2 axis should not be equated with CCL2 arm of pathway.

Keywords: peritoneal fibrosis, high glucose, TGF-beta1, Smad, CCL2, MCP-1, mesothelial-mesenchymal transition, PRISMA 2020, Vancouver references.

[PDF Full Text]