ReviewMolecular and cellular biochemistry2025
Phosphatase activity-based PPM1K: a key player in the regulation of mitochondrial function and its multifaceted impact in diseases.
Review in Molecular and cellular biochemistry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Aloe emodin attenuates AβOpen medicine (Warsaw, Poland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
PPM1K is a significant metal-dependent phosphatase predominantly located in the mitochondrial matrix, where it plays a crucial role in the metabolism of branched-chain amino acids (BCAAs). It is implicated in cellular function and development across various tissues and is associated with diseases like Alzheimer's, cardiomyopathy, and maple syrup urine disease (MSUD). This article reviews PPM1K's impact on mitochondrial function and cellular metabolism, as well as its role in disease progression. The regulation of PPM1K expression and activity by various factors is complex and highlights its therapeutic potential. PPM1K's dysfunction can lead to the accumulation of BCAAs and the excessive opening of the mitochondrial permeability transition pore (MPTP), disrupting physiological metabolism and function. It also regulates the degradation of BCAAs by acting as a specific phosphatase for the E1α subunit of the BCKD complex. Outside the mitochondria, PPM1K suppresses de novo fatty acid synthesis and promotes fatty acid oxidation by dephosphorylating ACL. Furthermore, PPM1K has anti-inflammatory effects and modulates immune cell infiltration in tumor tissues. The expression and activity of PPM1K are influenced by factors such as BCAA concentration, fructose intake, and drug treatments, making it a promising target for therapeutic applications and further basic research.
Indexed as
Identifiers
39695034What Socratic 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 Socratic graph.