The STAT3/JAK2 Signaling Pathway in Renal Fibrosis: Mechanistic Insights and Advances in Targeted Intervention
- 1College of Chinese Medicine
- 2Department of Endocrinology
Abstract
Yuxue Yu,1 Jiao Lv,1 Yilin Chai,1 Xiuge Wang,2 Miao Yu2 1College of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117, People’s Republic of China; 2Department of Endocrinology, First Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, 130021, People’s Republic of ChinaCorrespondence: Miao Yu; Xiuge Wang, Department of Endocrinology, First Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, 130021, People’s Republic of China, Email [email protected]; [email protected]: Renal fibrosis remains a major therapeutic challenge in chronic kidney disease. Evidence for therapies targeting signal transducer and activator of transcription 3 (STAT3) is predominantly preclinical, although Janus kinase (JAK) inhibitors have been evaluated in diabetic kidney disease. This review compares STAT3 signaling across acute kidney injury progressing to chronic disease, diabetes, hypertension, and hyperuricemic kidney injury. Cytokine receptors, growth-factor receptors, metabolic stress, and interorgan signals influence STAT3 activity in tubular, stromal, and immune cells. Their effects depend on cellular context, activation dynamics, and interactions with other fibrotic pathways. We distinguish pathway-associated changes from functional validation and direct target engagement when assessing synthetic inhibitors, cell-based therapies, and natural or traditional-medicine-derived interventions. Clinical albuminuria findings are considered separately from evidence of fibrosis regression. Priorities include cell-resolved pharmacodynamic markers, intervention windows defined by repair state, and evaluation of targeted delivery.Keywords: renal fibrosis, chronic kidney disease, JAK2/STAT3, maladaptive repair, targeted intervention
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BibTeX
@article{yu2026stat3jak2,
title = {{The STAT3/JAK2 Signaling Pathway in Renal Fibrosis: Mechanistic Insights and Advances in Targeted Intervention}},
author = {Yu Y and Lv J and Chai Y and Wang X and Yu M},
journal = {Journal of Inflammation Research},
year = {2026},
month = nov,
url = {https://www.dovepress.com/the-stat3jak2-signaling-pathway-in-renal-fibrosis-mechanistic-insights-peer-reviewed-fulltext-article-JIR},
note = {CC BY},
}
RIS
TY - JOUR
TI - The STAT3/JAK2 Signaling Pathway in Renal Fibrosis: Mechanistic Insights and Advances in Targeted Intervention
AU - Yu Y
AU - Lv J
AU - Chai Y
AU - Wang X
AU - Yu M
PY - 2026
DA - 2026/11/08
JO - Journal of Inflammation Research
UR - https://www.dovepress.com/the-stat3jak2-signaling-pathway-in-renal-fibrosis-mechanistic-insights-peer-reviewed-fulltext-article-JIR
AB - Yuxue Yu,1 Jiao Lv,1 Yilin Chai,1 Xiuge Wang,2 Miao Yu2 1College of Chinese Medicine, Changchun University of Chinese Medicine, Changchun, 130117, People’s Republic of China; 2Department of Endocrinology, First Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, 130021, People’s Republic of ChinaCorrespondence: Miao Yu; Xiuge Wang, Department of Endocrinology, First Affiliated Hospital to Changchun University of Chinese Medicine, Changchun, 130021, People’s Republic of China, Email [email protected]; [email protected]: Renal fibrosis remains a major therapeutic challenge in chronic kidney disease. Evidence for therapies targeting signal transducer and activator of transcription 3 (STAT3) is predominantly preclinical, although Janus kinase (JAK) inhibitors have been evaluated in diabetic kidney disease. This review compares STAT3 signaling across acute kidney injury progressing to chronic disease, diabetes, hypertension, and hyperuricemic kidney injury. Cytokine receptors, growth-factor receptors, metabolic stress, and interorgan signals influence STAT3 activity in tubular, stromal, and immune cells. Their effects depend on cellular context, activation dynamics, and interactions with other fibrotic pathways. We distinguish pathway-associated changes from functional validation and direct target engagement when assessing synthetic inhibitors, cell-based therapies, and natural or traditional-medicine-derived interventions. Clinical albuminuria findings are considered separately from evidence of fibrosis regression. Priorities include cell-resolved pharmacodynamic markers, intervention windows defined by repair state, and evaluation of targeted delivery.Keywords: renal fibrosis, chronic kidney disease, JAK2/STAT3, maladaptive repair, targeted intervention
SN - 1178-7031
ER -