ArticleMolecular medicine (Cambridge, Mass.)2023
Nicotine exacerbates diabetic nephropathy through upregulation of Grem1 expression.
Article in Molecular medicine (Cambridge, Mass.), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 10 citations in OpenAlex.
- Sex Differences in Albuminuria Risk with Metformin Use: Insights from a Cross-Sectional Study and Drug-Target Mendelian Randomization Analysis.Diabetes & metabolism journal · 2025Article
- Negative Air Ions Attenuate Nicotine-Induced Vascular Endothelial Dysfunction by Suppressing AP1-Mediated FN1 and SPP1.Antioxidants (Basel, Switzerland) · 2025Article
- Hydroxycotinine exhibits a stronger association with chronic kidney disease in smokers when compared to cotinine: Evidence from NHANES 2013-2018.Tobacco induced diseases · 2025Article
- Decreased Serum Adipose Triglyceride Lipase Level Is Associated With Renal Function Impairment in Patients With Type 2 Diabetes.Journal of diabetes research · 2025Article
- Association of Life's Essential 8 Score with All-Cause and Cardiovascular Mortality in Patients with Diabetic Nephropathy: A NHANES-Based Cohort Study.Journal of multidisciplinary healthcare · 2025Article
- Risk Factors for Cataracts in Patients with Diabetes Mellitus.Journal of clinical medicine · 2024Article
- The hidden impact: the rate of nicotine metabolism and kidney health.Frontiers in endocrinology · 2024Article
- The Molecular Mechanism of Renal Tubulointerstitial Inflammation Promoting Diabetic Nephropathy.International journal of nephrology and renovascular disease · 2023Review
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundDiabetic nephropathy (DN) is a major complication of diabetes mellitus. Clinical reports indicate that smoking is a significant risk factor for chronic kidney disease, and the tobacco epidemic exacerbates kidney damage in patients with DN. However, the underlying molecular mechanisms remain unclear.
methodIn the present study, we used a diabetic mouse model to investigate the molecular mechanisms for nicotine-exacerbated DN. Twelve-week-old female mice were injected with streptozotocin (STZ) to establish a hyperglycemic diabetic model. After four months, the control and hyperglycemic diabetic mice were further divided into four groups (control, nicotine, diabetic mellitus, nicotine + diabetic mellitus) by intraperitoneal injection of nicotine or PBS. After two months, urine and blood were collected for kidney injury assay, and renal tissues were harvested for further molecular assays using RNA-seq analysis, real-time PCR, Western blot, and immunohistochemistry. In vitro studies, we used siRNA to suppress Grem1 expression in human podocytes. Then we treated them with nicotine and high glucose to compare podocyte injury.
resultNicotine administration alone did not cause apparent kidney injury, but it significantly increased hyperglycemia-induced albuminuria, BUN, plasma creatinine, and the kidney tissue mRNA expression of KIM-1 and NGAL. Results from RNA-seq analysis, real-time PCR, Western blot, and immunohistochemistry analysis revealed that, compared to hyperglycemia or nicotine alone, the combination of nicotine treatment and hyperglycemia significantly increased the expression of Grem1 and worsened DN. In vitro experiments, suppression of Grem1 expression attenuated nicotine-exacerbated podocyte injury.
conclusionGrem1 plays a vital role in nicotine-exacerbated DN. Grem1 may be a potential therapeutic target for chronic smokers with DN.
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