Periostin in diabetic kidney disease: mechanistic insights, biomarkers, and therapeutic perspectives
- 1The Fourth Clinical Medical College of Guangzhou University of Chinese Medicine
- 2Department of Nephrology, Shenzhen Traditional Chinese Medicine Hospital
Abstract
Diabetic kidney disease (DKD) is among the most common and severe microvascular complications of diabetes and represents a leading cause of end-stage renal disease (ESRD) worldwide. Currently, although strict glycemic and blood pressure control, together with the use of renin–angiotensin system inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and non-steroidal selective mineralocorticoid receptor antagonists, can moderately delay DKD progression, the risks of progression to ESRD and cardiovascular events remain high, highlighting the urgent need to identify novel therapeutic targets. Preclinical and observational studies suggest that periostin (POSTN) is associated with DKD progression and may contribute to renal inflammation and fibrosis. POSTN expression is minimal in healthy kidneys but is markedly upregulated under conditions of renal injury and fibrosis. Cross-sectional clinical studies report that serum, urinary, and renal tissue POSTN levels are elevated in patients with DKD and correlate with proteinuria, the severity of renal fibrosis, and a decline in estimated glomerular filtration rate (eGFR); these associations have not been confirmed prospectively. Preclinical studies indicate that POSTN promotes inflammatory cell infiltration, myofibroblast activation, and extracellular matrix accumulation, and it has therefore been proposed to contribute to the inflammatory and fibrotic progression of DKD. In preclinical DKD models, POSTN inhibition attenuates renal injury and fibrosis. No POSTN-targeted therapy has entered human clinical trials, so POSTN remains a promising preclinical candidate target. This review summarizes the mechanistic basis and recent advances in POSTN research in DKD, and further explores its translational potential as a biomarker and therapeutic target.
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BibTeX
@article{li2026periostin,
title = {{Periostin in diabetic kidney disease: mechanistic insights, biomarkers, and therapeutic perspectives}},
author = {Xuhao Li and Yamiao Wu and Yexuan Shi and Guoliang Xiong and Lingfei Lu and Jiandong Lu},
journal = {Frontiers in Endocrinology},
year = {2026},
month = oct,
doi = {10.3389/fendo.2026.1979232},
url = {https://www.frontiersin.org/articles/10.3389/fendo.2026.1979232/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Periostin in diabetic kidney disease: mechanistic insights, biomarkers, and therapeutic perspectives
AU - Xuhao Li
AU - Yamiao Wu
AU - Yexuan Shi
AU - Guoliang Xiong
AU - Lingfei Lu
AU - Jiandong Lu
PY - 2026
DA - 2026/10/09
JO - Frontiers in Endocrinology
DO - 10.3389/fendo.2026.1979232
UR - https://www.frontiersin.org/articles/10.3389/fendo.2026.1979232/full
AB - Diabetic kidney disease (DKD) is among the most common and severe microvascular complications of diabetes and represents a leading cause of end-stage renal disease (ESRD) worldwide. Currently, although strict glycemic and blood pressure control, together with the use of renin–angiotensin system inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, glucagon-like peptide-1 (GLP-1) receptor agonists, and non-steroidal selective mineralocorticoid receptor antagonists, can moderately delay DKD progression, the risks of progression to ESRD and cardiovascular events remain high, highlighting the urgent need to identify novel therapeutic targets. Preclinical and observational studies suggest that periostin (POSTN) is associated with DKD progression and may contribute to renal inflammation and fibrosis. POSTN expression is minimal in healthy kidneys but is markedly upregulated under conditions of renal injury and fibrosis. Cross-sectional clinical studies report that serum, urinary, and renal tissue POSTN levels are elevated in patients with DKD and correlate with proteinuria, the severity of renal fibrosis, and a decline in estimated glomerular filtration rate (eGFR); these associations have not been confirmed prospectively. Preclinical studies indicate that POSTN promotes inflammatory cell infiltration, myofibroblast activation, and extracellular matrix accumulation, and it has therefore been proposed to contribute to the inflammatory and fibrotic progression of DKD. In preclinical DKD models, POSTN inhibition attenuates renal injury and fibrosis. No POSTN-targeted therapy has entered human clinical trials, so POSTN remains a promising preclinical candidate target. This review summarizes the mechanistic basis and recent advances in POSTN research in DKD, and further explores its translational potential as a biomarker and therapeutic target.
SN - 1664-2392
ER -