Component

Mitochondrial NAD+ content

Measured amount or biosensor-defined availability of NAD+ in mitochondria; not total cellular NAD.

4 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Overexpression of human SLC25A52 increased mitochondrial NAD+ in cultured human cells and complemented yeast lacking endogenous mitochondrial NAD transporters.

    Human SLC25A52 → Mitochondrial NAD+ content source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human-cell overexpression and yeast complementation.
    limitations
    Overexpression does not establish normal tissue contribution, redundancy or human treatment efficacy.
    nutrient_topic
    NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+
    plain_language
    A related transporter can support mitochondrial NAD availability in experimental systems.
    primary_references
    SLC25A51 is a mammalian mitochondrial NAD+ transporter. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32906142/ · DOI 10.1038/s41586-020-2741-7

    NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 44–50

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human-cell overexpression and yeast complementation. · source_derived_draft · unverified_draft

    ## nad-plus-slc52-expression A related transporter can support mitochondrial NAD availability in experimental systems. Overexpression of human SLC25A52 increased mitochondrial NAD+ in cultured human cells and complemented yeast lacking endogenous mitochondrial NAD transporters. Model: Human-cell overexpression and yeast complementation. Limitations: Overexpression does not establish normal tissue contribution, redundancy or human treatment efficacy. Evidence access: Primary full text SLC25A51 is a mammalian mitochondrial NAD+ transporter. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32906142/ · DOI 10.1038/s41586-020-2741-7
    Complete structured claim and evidence

  2. SLC25A51 loss reduced mitochondrial NAD+ availability in the tested human cell models.

    SLC25A51 depletion or knockout → Mitochondrial NAD+ content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 6119, "end_char": 6538, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "024f4688a65e3279f2865ef892f19ed4d5357469c71a5e2e6fb27fe1a2dd4043"}
    experimental_model
    Multiple shRNA/siRNA perturbations; mitochondrial assays and biosensors
    exposure
    SLC25A51 RNA interference
    limitations
    Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Cells can lose mitochondrial NAD even when the total-cell pool is maintained.
    primary_references
    [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
    tissue_or_cell_type
    Human cultured cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1042–1053

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multiple shRNA/siRNA perturbations; mitochondrial assays and biosensors · source_derived_draft · unverified_draft

    ### b3-redox-slc25a51-mito-pool SLC25A51 loss reduced mitochondrial NAD+ availability in the tested human cell models. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells can lose mitochondrial NAD even when the total-cell pool is maintained. organism: Homo sapiens tissue_or_cell_type: Human cultured cells experimental_model: Multiple shRNA/siRNA perturbations; mitochondrial assays and biosensors limitations: Scoped experimental observation; no dietary niacin or magnesium deficiency threshold or treatment benefit was tested. exposure: SLC25A51 RNA interference evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 6119, "end_char": 6538, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "024f4688a65e3279f2865ef892f19ed4d5357469c71a5e2e6fb27fe1a2dd4043"} [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
    Complete structured claim and evidence

  3. Unlike NAD+, exogenous nicotinamide or NMN did not replenish matrix NAD+ in the isolated-mitochondrial assay.

    Nicotinamide → Mitochondrial NAD+ content source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 18765, "end_char": 19225, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "121f48fd5cc272acc24a9ca1610c801423a98e3e44f7851e649c8454750e7fb0"}
    experimental_model
    Isolated mitochondria substrate comparison
    exposure
    Exogenous NAD+, nicotinamide or NMN
    limitations
    Does not imply oral NAM/NMN cannot contribute to mitochondrial NAD after extramitochondrial metabolism; this is an isolated-organelle test.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    These precursors were not interchangeable with intact NAD in this uptake experiment.
    primary_references
    [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
    tissue_or_cell_type
    Isolated human-cell mitochondria

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1068–1079

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated mitochondria substrate comparison · source_derived_draft · unverified_draft

    ### b3-redox-slc25a51-nam-nmn-null Unlike NAD+, exogenous nicotinamide or NMN did not replenish matrix NAD+ in the isolated-mitochondrial assay. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: These precursors were not interchangeable with intact NAD in this uptake experiment. organism: Homo sapiens tissue_or_cell_type: Isolated human-cell mitochondria experimental_model: Isolated mitochondria substrate comparison limitations: Does not imply oral NAM/NMN cannot contribute to mitochondrial NAD after extramitochondrial metabolism; this is an isolated-organelle test. exposure: Exogenous NAD+, nicotinamide or NMN evidence_span: {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 18765, "end_char": 19225, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "121f48fd5cc272acc24a9ca1610c801423a98e3e44f7851e649c8454750e7fb0"} [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
    Complete structured claim and evidence

  4. Restoration of mitochondrial NAD+ by nicotinamide riboside in the intact-cell biosensor experiment depended on SLC25A51.

    SLC25A51 → Mitochondrial NAD+ content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    [{"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 19922, "end_char": 20160, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "78e9cfd3c25b8d33b54ac67bebc01314eed3925b3b6a4bdea527d48191da0977"}, {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 24477, "end_char": 24725, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "7125713c87024da0a0f8c1d4442115144c9ff20543fbd39cfc4cfc46de135cad"}]
    experimental_model
    HeLa siRNA and mitochondrial NAD biosensor
    exposure
    100 μM NR for 16 h after siRNA transfection three days earlier
    limitations
    Cultured-cell precursor response; no direct clinical inference or generic claim that every NAD-raising intervention fails.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Homo sapiens
    plain_language
    Precursor provision still required functional mitochondrial import in these cells.
    primary_references
    [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
    tissue_or_cell_type
    HeLa cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1094–1105

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HeLa siRNA and mitochondrial NAD biosensor · source_derived_draft · unverified_draft

    ### b3-redox-slc25a51-nr-dependence Restoration of mitochondrial NAD+ by nicotinamide riboside in the intact-cell biosensor experiment depended on SLC25A51. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Precursor provision still required functional mitochondrial import in these cells. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: HeLa siRNA and mitochondrial NAD biosensor limitations: Cultured-cell precursor response; no direct clinical inference or generic claim that every NAD-raising intervention fails. exposure: 100 μM NR for 16 h after siRNA transfection three days earlier evidence_span: [{"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 19922, "end_char": 20160, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "78e9cfd3c25b8d33b54ac67bebc01314eed3925b3b6a4bdea527d48191da0977"}, {"source_cache": "artifacts/niacin-redox-sources/slc25a51-2020.author.txt", "locator": "Publisher PDF, results; page/figure identified by adjacent text", "start_char": 24477, "end_char": 24725, "file_sha256": "8348dbfda6d16d576bb64301f0c75f1488e90e33c4a72213b69756bed21d047d", "text_sha256": "7125713c87024da0a0f8c1d4442115144c9ff20543fbd39cfc4cfc46de135cad"}] [slc25a51-2020] SLC25A51 is a mammalian mitochondrial NAD+ transporter. (2020). https://pubmed.ncbi.nlm.nih.gov/32906142/ DOI: 10.1038/s41586-020-2741-7
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards