ArticleAmerican journal of translational research2018
MnTBAP treatment ameliorates aldosterone-induced renal injury by regulating mitochondrial dysfunction and NLRP3 inflammasome signalling.
Article in American journal of translational research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 13 citations in OpenAlex.
- Manganese (III) tetrakis (4-benzoic acid) porphyrin (MnTBAP) represses sulfide:quinone oxidoreductase expression and targets the sulfido-redox system in glioblastoma models.Redox report : communications in free radical research · 2025Article
- Depletion of WFS1 compromises mitochondrial function in hiPSC-derived neuronal models of Wolfram syndrome.Stem cell reports · 2023Article
- Leonurine attenuates cisplatin nephrotoxicity by suppressing the NLRP3 inflammasome, mitochondrial dysfunction, and endoplasmic reticulum stress.International urology and nephrology · 2022Article
- Impact of MnTBAP and Baricitinib Treatment on Hutchinson-Gilford Progeria Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Hormonal Regulation of Renal Fibrosis.Life (Basel, Switzerland) · 2022Review
- Catalytic Antioxidants in the Kidney.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial DNA-Mediated Inflammation in Acute Kidney Injury and Chronic Kidney Disease.Oxidative medicine and cellular longevity · 2021Review
- MnTBAP Reverses Pulmonary Vascular Remodeling and Improves Cardiac Function in Experimentally Induced Pulmonary Arterial Hypertension.International journal of molecular sciences · 2020Article
- Role of Inflammasomes in Kidney Diseases via Both Canonical and Non-canonical Pathways.Frontiers in cell and developmental biology · 2020Review
Corrections and comments
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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
Aldosterone plays an important role in the pathogenesis of chronic kidney disease (CKD) by directly damaging renal tubular cells. However, the treatment against aldosterone-induced renal injury is still limited. The present study was performed to examine the protection role of MnTBAP in modulating aldosterone-induced renal tubular injury both in vitro and vivo. MtD is induced by aldosterone in HK-2 cells, as evidenced by decreased expression of mtDNA and reduced mitochondrial membrane potential (MMP), which was markedly ameliorated by treatment with MnTBAP. HK-2 cells treated with MnTBAP demonstrated a reduction in cell apoptosis and improvements in cell phenotypic alterations following aldosterone challenge. Treatment with MnTBAP also inhibited the activation of the NLRP3 inflammasome and subsequent release of pro-inflammatory cytokines, IL-1β and IL-18. In addition, MnTBAP treatment of aldosterone-infused mice significantly improved mitochondrial morphology and function, suppressed the activation of NLRP3 inflammasome, reduced renal tubular cell apoptosis, decreased phenotypic alterations, and ameliorated renal apoptosis. We conclude that MnTBAP treatment ameliorates aldosterone-induced renal injury through regulating MtD and NLRP3 inflammsome signalling axis.
Indexed as
Identifiers
30662603PMC6291724W2997094230What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.