ArticleAmerican journal of physiology. Lung cellular and molecular physiology2014
MKK3 regulates mitochondrial biogenesis and mitophagy in sepsis-induced lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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Who cites it
57 citing papers in PubMed, 95 citations in OpenAlex.
- PRKN Ser131 phosphorylation promotes cigarette smoke-induced mitophagy impairment and epithelial cell senescence via MKK3/p38 MAPK activation: An in vitro and in vivo study.Tobacco induced diseases · 2026Article
- Sirtuins in mitophagy: key gatekeepers of mitochondrial quality.Molecular and cellular biochemistry · 2025Review
- Metabolic reprogramming of macrophages in chronic obstructive pulmonary disease.Frontiers in immunology · 2025Review
- Molecular mechanism and potential role of mitophagy in acute pancreatitis.Molecular medicine (Cambridge, Mass.) · 2024Review
- HSPB8 attenuates lipopolysaccharide‑mediated acute lung injury in A549 cells by activating mitophagy.Molecular medicine reports · 2024Article
- MKK3 depletion attenuates intestinal injury after traumatic hemorrhagic shock by restoring mitochondrial function.Molecular biology reports · 2024Article
- Circulating N-lactoyl-amino acids and N-formyl-methionine reflect mitochondrial dysfunction and predict mortality in septic shock.Metabolomics : Official journal of the Metabolomic Society · 2024Article
- Peroxiredoxin 3 has a crucial role in the macrophage polarization by regulating mitochondrial homeostasis.Respiratory research · 2024Article
- Pyruvate kinase M2 sustains cardiac mitochondrial integrity in septic cardiomyopathy by regulating PHB2-dependent mitochondrial biogenesis.International journal of medical sciences · 2024Article
- Restoring the infected powerhouse: Mitochondrial quality control in sepsis.Redox biology · 2023Review
- Crosstalk between mitochondrial biogenesis and mitophagy to maintain mitochondrial homeostasis.Journal of biomedical science · 2023Review
- Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review.Antioxidants (Basel, Switzerland) · 2023Review
- The mitophagy pathway and its implications in human diseases.Signal transduction and targeted therapy · 2023Review
- SH2 Domain-Containing Phosphatase-SHP2 Attenuates Fibrotic Responses through Negative Regulation of Mitochondrial Metabolism in Lung Fibroblasts.Diagnostics (Basel, Switzerland) · 2023Article
- Melatonin Attenuates Sepsis-Induced Acute Lung Injury via Inhibiting Excessive Mitophagy.Drug design, development and therapy · 2023Article
- RCAN1 deficiency aggravates sepsis-induced cardiac remodeling and dysfunction by accelerating mitochondrial pathological fission.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022Article
- Mitochondria and their potential role in acute lung injury (Review).Experimental and therapeutic medicine · 2022Review
- Hydrogen alleviates cell damage and acute lung injury in sepsis via PINK1/Parkin-mediated mitophagy.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021Article
- Mediators of mitophagy that regulate mitochondrial quality control play crucial role in diverse pathophysiology.Cell biology and toxicology · 2021Review
- Post-translational regulation of PGC-1α modulates fibrotic repair.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
Corrections and comments
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Sepsis is a systemic inflammatory response to infection and a major cause of death worldwide. Because specific therapies to treat sepsis are limited, and underlying pathogenesis is unclear, current medical care remains purely supportive. Therefore targeted therapies to treat sepsis need to be developed. Although an important mediator of sepsis is thought to be mitochondrial dysfunction, the underlying molecular mechanism is unclear. Modulation of mitochondrial processes may be an effective therapeutic strategy in sepsis. Here, we investigated the role of the kinase MKK3 in regulation of mitochondrial function in sepsis. Using clinically relevant animal models, we examined mitochondrial function in primary mouse lung endothelial cells exposed to LPS. MKK3 deficiency reduces lethality of sepsis in mice and by lowering levels of lung and mitochondrial injury as well as reactive oxygen species. Furthermore, MKK3 deficiency appeared to simultaneously increase mitochondrial biogenesis and mitophagy through the actions of Sirt1, Pink1, and Parkin. This led to a more robust mitochondrial network, which we propose provides protection against sepsis. We also detected higher MKK3 activation in isolated peripheral blood mononuclear cells from septic patients compared with nonseptic controls. Our findings demonstrate a critical role for mitochondria in the pathogenesis of sepsis that involves a previously unrecognized function of MKK3 in mitochondrial quality control. This mitochondrial pathway may help reveal new diagnostic markers and therapeutic targets against sepsis.
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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.