ArticleBioengineered2022
Sp1 transcription factor represses transcription of phosphatase and tensin homolog to aggravate lung injury in mice with type 2 diabetes mellitus-pulmonary tuberculosis.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Screening and predictive analysis of common regulatory genes in diabetes and rectal cancer: transcriptional and drug modulation mechanisms.European journal of medical research · 2025Article
- Article
- PTEN in kidney diseases: a potential therapeutic target in preventing AKI-to-CKD transition.Frontiers in medicine · 2024Review
- Unraveling genetic causality between type 2 diabetes and pulmonary tuberculosis on the basis of Mendelian randomization.Diabetology & metabolic syndrome · 2023Article
- Intervention Effects of Physical Activity on Type 2 Diabetic Patients Potentially Infected with COVID-19.Medicina (Kaunas, Lithuania) · 2023Review
- Host-directed therapy against mycobacterium tuberculosis infections with diabetes mellitus.Frontiers in immunology · 2023Review
- CircUBXN7 promotes macrophage infiltration and renal fibrosis associated with the IGF2BP2-dependent SP1 mRNA stability in diabetic kidney disease.Frontiers in immunology · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 2 diabetes mellitus (T2DM) can enhance the risk of mycobacterium tuberculosis (Mtb) infection and aggravate pulmonary tuberculosis (PTB). This study intended to explore the function of phosphatase and tensin homolog (PTEN) in T2DM-PTB and the molecules involved. Mice were treated with streptozotocin to induce T2DM and then infected with Mtb. The mice with T2DM had increased weight, blood glucose level, glucose intolerance and insulin resistance, and increased susceptibility to PTB after Mtb infection. PTEN was significantly downregulated in mice with T2DM-PTB and it had specific predictive value in patients. Overexpression of PTEN improved mouse survival and reduced bacterial load, inflammatory infiltration, cell apoptosis, and fibrosis in lung tissues. Sp1 transcription factor (SP1) was predicted and identified as an upstream regulator of PTEN. SP1 suppressed PTEN transcription. Silencing of SP1 enhanced mouse survival and alleviated the lung injury, and it promoted the M1 polarization of macrophages in murine lung tissues. However, further downregulation of PTEN increased protein kinase B (Akt) phosphorylation and blocked the alleviating roles of SP1 silencing in T2DM-PTB. This study demonstrates that SP1 represses PTEN transcription to promote lung injury in mice with T2DM-PTB through Akt activation.
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