Longitudinal assessment of bleomycin-induced pulmonary fibrosis by evaluating TGF-β1/Smad2, Nrf2 signaling and metabolomic analysis in mice

Washimkar, Kaveri R.; Tomar, Manendra Singh; Kulkarni, Chirag; Verma, Shobhit; Shrivastava, Ashutosh; Chattopadhyay, Naibedya; Mugale, Madhav Nilakanth

doi:10.1016/j.lfs.2023.122064

Life Sciences

2023

DOI: 10.1016/j.lfs.2023.122064

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Longitudinal assessment of bleomycin-induced pulmonary fibrosis by evaluating TGF-β1/Smad2, Nrf2 signaling and metabolomic analysis in mice

Kaveri R. Washimkar,

Manendra Singh Tomar,

Chirag Kulkarni

et al.

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2024

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Cited by 6 publications

References 70 publications

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Unraveling the interplay between vital organelle stress and oxidative stress in idiopathic pulmonary fibrosis

Mohanan,

Washimkar,

Mugale

2024

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Unraveling the interplay between vital organelle stress and oxidative stress in idiopathic pulmonary fibrosis

Mohanan,

Washimkar,

Mugale

2024

Biochimica et Biophysica Acta (BBA) - Molecular Cell Research

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Immune cells crosstalk Pathways, and metabolic alterations in Idiopathic pulmonary fibrosis

Tiwari,

Verma,

Washimkar

et al. 2024

International Immunopharmacology

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SGLT2i improves kidney senescence by down‐regulating the expression of LTBP2 in SAMP8 mice

Zeng,

Li,

Gao

et al. 2024

J Cellular Molecular Medi

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Senescent kidney can lead to the maladaptive repairment and predispose age‐related kidney diseases. Here, we explore the renal anti‐senescence effect of a known kind of drug, sodium‐dependent glucose transporters 2 inhibitor (SGLT2i). After 4 months intragastrically administration with dapagliflozin on senescence‐accelerated mouse prone 8 (SAMP8) strain mice, the physiologically effects (lowering urine protein, enhancing glomerular blood perfusion, inhibiting expression of senescence‐related biomarkers) and structural changes (improving kidney atrophy, alleviating fibrosis, decreasing glomerular mesangial proliferation) indicate the potential value of delaying kidney senescence of SGLT2i. Senescent human proximal tubular epithelial (HK‐2) cells induced by H2O2 also exhibit lower senescent markers after dapagliflozin treatment. Further mechanism exploration suggests LTBP2 have the great possibility to be the target for SGLT2i to exert its renal anti‐senescence role. Dapagliflozin down‐regulate the LTBP2 expression in kidney tissues and HK‐2 cells with senescent phenotypes. Immunofluorescence staining show SGLT2 and LTBP2 exist colocalization, and protein‐docking analysis implies there is salt‐bridge formation between them; these all indicate the possibility of weak‐interaction between the two proteins. Apart from reducing LTBP2 expression in intracellular area induced by H2O2, dapagliflozin also decrease the concentration of LTBP2 in cell culture medium. Together, these results reveal dapagliflozin can delay natural kidney senescence in non‐diabetes environment; the mechanism may be through regulating the role of LTBP2.

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Longitudinal assessment of bleomycin-induced pulmonary fibrosis by evaluating TGF-β1/Smad2, Nrf2 signaling and metabolomic analysis in mice

Cited by 6 publications

References 70 publications

Unraveling the interplay between vital organelle stress and oxidative stress in idiopathic pulmonary fibrosis

Unraveling the interplay between vital organelle stress and oxidative stress in idiopathic pulmonary fibrosis

Immune cells crosstalk Pathways, and metabolic alterations in Idiopathic pulmonary fibrosis

SGLT2i improves kidney senescence by down‐regulating the expression of LTBP2 in SAMP8 mice

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