Notch3 deletion regulates HIV-1 gene expression and systemic inflammation to ameliorate chronic kidney disease.
Mackenzie ThorntonNicole SommerMercedes McGonigleAnil Kumar RamSireesha YerrathotaHenrietta EhirimAakriti ChaturvediJohnny Dinh PhanPraveen V ChakravarthiSumedha GunewardenaJaya TalrejaPravin SinghalTimothy A FieldsPatricio E RayNavneet K DhillonMadhulika SharmaPublished in: bioRxiv : the preprint server for biology (2023)
Notch3 inhibition has been reported to be an anti-inflammatory strategy for glomerular diseases. Here, using an HIV-1 transgenic mouse model we show that global Notch3 deletion not only improves kidney phenotype but also renal expression of HIV gene, Nef and systemic inflammation which leads to a drastic increase of life span of these mice. Notch3 inhibition can thus play a dual protective role in HIV related chronic diseases.
Keyphrases
- antiretroviral therapy
- hiv positive
- hiv testing
- hiv infected
- human immunodeficiency virus
- hepatitis c virus
- hiv aids
- men who have sex with men
- gene expression
- chronic kidney disease
- cell proliferation
- mouse model
- anti inflammatory
- poor prognosis
- south africa
- skeletal muscle
- transcription factor
- endothelial cells
- adipose tissue