ArticleBiochimica et biophysica acta. Molecular basis of disease2017
Surfactant protein A deficiency exacerbates renal interstitial fibrosis following obstructive injury in mice.
Article in Biochimica et biophysica acta. Molecular basis of disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Roles of sex and SP-A genetic variants in modulating multiorgan injuries post viral infection.Frontiers in immunology · 2026Article
- High Mobility Group Box 1 (HMGB1): Molecular Signaling and Potential Therapeutic Strategies.Cells · 2024Review
- Surfactant protein a attenuates generalized and localized neuroinflammation in neonatal mice.Brain research · 2023Article
- Targeting HMGB1: A Potential Therapeutic Strategy for Chronic Kidney Disease.International journal of biological sciences · 2023Review
- Regulatory roles of SP-A and exosomes in pneumonia-induced acute lung and kidney injuries.Frontiers in immunology · 2023Article
- Targeting CC chemokine ligand (CCL) 20 by miR-143-5p alleviate lead poisoning-induced renal fibrosis by regulating interstitial fibroblasts excessive proliferation and dysfunction.Bioengineered · 2022Article
- Examination of the role of necroptotic damage-associated molecular patterns in tissue fibrosis.Frontiers in immunology · 2022Review
- GSDME-mediated pyroptosis promotes inflammation and fibrosis in obstructive nephropathy.Cell death and differentiation · 2021Article
- Surfactant Protein A, a Novel Regulator for Smooth Muscle Phenotypic Modulation and Vascular Remodeling-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2021Article
- Recent progress on surfactant protein A: cellular function in lung and kidney disease development.American journal of physiology. Cell physiology · 2020Review
- DAMPs in Unilateral Ureteral Obstruction.Frontiers in immunology · 2020Review
- Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin.Experimental and therapeutic medicine · 2019Article
- Collectins in urinary tract and kidney diseases.International urology and nephrology · 2018Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Renal interstitial fibrosis is an inevitable consequence of virtually every type of chronic kidney disease. The underlying mechanisms, however, are not completely understood. In the present study, we identified surfactant protein A (SP-A) as a novel protein factor involved in the renal fibrosis induced by unilateral ureter obstruction (UUO). UUO induced SP-A expression in mouse kidney epithelium, likely due to the increased acidic stress and inflammation. Interestingly, SP-A deficiency aggravated UUO-prompted kidney structural damage, macrophage accumulation, and tubulointerstitial fibrosis. SP-A deficiency appeared to worsen the fibrosis by enhancing interstitial myofibroblast accumulation. Moreover, SP-A deficiency increased the expression of TGF-β1, the major regulator of kidney fibrosis, particularly in the interstitial cells. Mechanistically, SP-A deficiency increased the expression and release of high mobility group box 1 (HMGB1), a factor regulating TGF-β expression/signaling and implicated in renal fibrosis. SP-A also blocked HMGB1 activities in inducing TGF-β1 expression and myofibroblast transdifferentiation from kidney fibroblasts, demonstrating that SP-A protected kidney by impeding both the expression and fibrogenic function of HMGB1. Since SP-A physically interacted with HMGB1 both in vitro and in kidney tissue in vivo, SP-A may exert its protective role by binding to HMGB1 and thus titrating its activity during UUO-induced renal fibrosis.
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