Mitochondrial Proteostasis Coupling Therapy

From Analysis:

How do host cell factors influence the conformation and propagation properties of transmitted pathological seeds?

The abstract acknowledges that host cells influence seed properties, but the specific cellular factors and mechanisms involved are not well understood. This knowledge gap limits our ability to predict disease progression and develop cell-targeted therapies. Gap type: open_question Source paper: Protein transmission in neurodegenerative disease. (2020, Nat Rev Neurol, PMID:32203399)

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graph TD
    ATP6V1A["ATP6V1A"] -->|encodes subunit of| v_ATPase["v-ATPase"]
    ATP6V1A_1["ATP6V1A"] -->|encodes subunit of| lysosomal_acidification["lysosomal acidification"]
    v_ATPase_2["v-ATPase"] -->|modulates| lysosomal_pH["lysosomal pH"]
    lysosomal_acidification_3["lysosomal acidification"] -->|enables| protein_degradation["protein degradation"]
    protein_degradation_4["protein degradation"] -->|protects against| neurodegeneration["neurodegeneration"]
    ATF5["ATF5"] -->|transcriptional ac| UPRmt["UPRmt"]
    UPRmt_5["UPRmt"] -->|regulates| mitochondrial_proteostasi["mitochondrial proteostasis"]
    mitochondrial_proteostasi_6["mitochondrial proteostasis"] -->|resists| seed_induced_protein_misf["seed-induced protein misfolding"]
    HSPA1A["HSPA1A"] -->|facilitates| protein_folding["protein folding"]
    HSPA1A_7["HSPA1A"] -->|enhances| chaperone_co_chaperone_co["chaperone-co-chaperone complexes"]
    protein_folding_8["protein folding"] -->|prevents| protein_aggregation["protein aggregation"]
    pathological_conformation["pathological conformations"] -->|converts| benign_or_degradable_form["benign or degradable forms"]
    style ATP6V1A fill:#ce93d8,stroke:#333,color:#000
    style v_ATPase fill:#4fc3f7,stroke:#333,color:#000
    style ATP6V1A_1 fill:#ce93d8,stroke:#333,color:#000
    style lysosomal_acidification fill:#81c784,stroke:#333,color:#000
    style v_ATPase_2 fill:#4fc3f7,stroke:#333,color:#000
    style lysosomal_pH fill:#4fc3f7,stroke:#333,color:#000
    style lysosomal_acidification_3 fill:#81c784,stroke:#333,color:#000
    style protein_degradation fill:#4fc3f7,stroke:#333,color:#000
    style protein_degradation_4 fill:#4fc3f7,stroke:#333,color:#000
    style neurodegeneration fill:#ef5350,stroke:#333,color:#000
    style ATF5 fill:#ce93d8,stroke:#333,color:#000
    style UPRmt fill:#81c784,stroke:#333,color:#000
    style UPRmt_5 fill:#81c784,stroke:#333,color:#000
    style mitochondrial_proteostasi fill:#4fc3f7,stroke:#333,color:#000
    style mitochondrial_proteostasi_6 fill:#4fc3f7,stroke:#333,color:#000
    style seed_induced_protein_misf fill:#4fc3f7,stroke:#333,color:#000
    style HSPA1A fill:#ce93d8,stroke:#333,color:#000
    style protein_folding fill:#4fc3f7,stroke:#333,color:#000
    style HSPA1A_7 fill:#ce93d8,stroke:#333,color:#000
    style chaperone_co_chaperone_co fill:#4fc3f7,stroke:#333,color:#000
    style protein_folding_8 fill:#4fc3f7,stroke:#333,color:#000
    style protein_aggregation fill:#4fc3f7,stroke:#333,color:#000
    style pathological_conformation fill:#4fc3f7,stroke:#333,color:#000
    style benign_or_degradable_form fill:#4fc3f7,stroke:#333,color:#000

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