Component
Mouse mitochondrial amidoxime-reducing component 1 / Mtarc1
Mouse mitochondrial amidoxime-reducing component 1 / Mtarc1. Species, exposure and limitations are retained in each linked claim.
6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Whole-body Marc1 knockout did not protect against hepatic triglyceride accumulation, inflammation or fibrosis in this mouse study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/38437227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b", "start_char": 0, "end_char": 1333, "text_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b"}
- experimental_model
- Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout
- exposure
- MARC1 variants and mouse global knockout
- limitations
- Human association and mouse intervention are separate. The knockout null result differs from later published mouse knockout protection.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Human genetics in about 540000 individuals; Mus musculus knockout
- plain_language
- Removing MTARC1 did not help in this experiment.
- primary_references
- [mo-p38437227] Divergent role of Mitochondrial Amidoxime Reducing Component 1 (MARC1) in human and mouse. (2024). https://pubmed.ncbi.nlm.nih.gov/38437227/ DOI: 10.1371/journal.pgen.1011179
- tissue_or_cell_type
- Liver phenotypes
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1509–1520
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout · source_derived_draft · unverified_draft
### mo-marc-ko-null Whole-body Marc1 knockout did not protect against hepatic triglyceride accumulation, inflammation or fibrosis in this mouse study. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing MTARC1 did not help in this experiment. organism: Human genetics in about 540000 individuals; Mus musculus knockout tissue_or_cell_type: Liver phenotypes experimental_model: Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout limitations: Human association and mouse intervention are separate. The knockout null result differs from later published mouse knockout protection. exposure: MARC1 variants and mouse global knockout evidence_span: {"source_cache": "artifacts/molybdenum-research/38437227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b", "start_char": 0, "end_char": 1333, "text_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b"} [mo-p38437227] Divergent role of Mitochondrial Amidoxime Reducing Component 1 (MARC1) in human and mouse. (2024). https://pubmed.ncbi.nlm.nih.gov/38437227/ DOI: 10.1371/journal.pgen.1011179
Complete structured claim and evidenceGlobal deletion and hepatocyte-specific knockdown of Mtarc1 reduced steatosis and fibrosis in multiple mouse models.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/39927988.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d", "start_char": 0, "end_char": 1938, "text_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d"}
- experimental_model
- Global deletion and hepatocyte-specific knockdown across mouse MASH/fibrosis models; cellular variants
- exposure
- Mtarc1 depletion under lipotoxic and diet/fibrosis challenges
- limitations
- Preclinical protein-targeting study. A165T retained mitochondrial localization in these experiments, unlike the endogenous HepG2 study; construct/model effects remain unresolved.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Mus musculus; human variant cell experiments
- plain_language
- Removing MTARC1 helped in these experiments.
- primary_references
- [mo-p39927988] Loss of mitochondrial amidoxime-reducing component 1 (mARC1) prevents disease progression by reducing fibrosis in multiple mouse models of chronic liver disease. (2025). https://pubmed.ncbi.nlm.nih.gov/39927988/ DOI: 10.1097/hc9.0000000000000637
- tissue_or_cell_type
- Liver and hepatocytes
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1535–1546
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Global deletion and hepatocyte-specific knockdown across mouse MASH/fibrosis models; cellular variants · source_derived_draft · unverified_draft
### mo-marc-ko-protection-2025 Global deletion and hepatocyte-specific knockdown of Mtarc1 reduced steatosis and fibrosis in multiple mouse models. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing MTARC1 helped in these experiments. organism: Mus musculus; human variant cell experiments tissue_or_cell_type: Liver and hepatocytes experimental_model: Global deletion and hepatocyte-specific knockdown across mouse MASH/fibrosis models; cellular variants limitations: Preclinical protein-targeting study. A165T retained mitochondrial localization in these experiments, unlike the endogenous HepG2 study; construct/model effects remain unresolved. exposure: Mtarc1 depletion under lipotoxic and diet/fibrosis challenges evidence_span: {"source_cache": "artifacts/molybdenum-research/39927988.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d", "start_char": 0, "end_char": 1938, "text_sha256": "0ac1fb695999e1691580706469d581ce6bd90eeab03f7c26c1c79fbb4b4e169d"} [mo-p39927988] Loss of mitochondrial amidoxime-reducing component 1 (mARC1) prevents disease progression by reducing fibrosis in multiple mouse models of chronic liver disease. (2025). https://pubmed.ncbi.nlm.nih.gov/39927988/ DOI: 10.1097/hc9.0000000000000637
Complete structured claim and evidenceGlobal and liver-specific Mtarc1 knockout protected against diet-induced triglyceride accumulation, inflammation and fibrosis.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"}
- experimental_model
- Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions
- exposure
- Diet-induced liver disease with gene knockouts/knockdowns and multi-omics
- limitations
- Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Mus musculus; supporting cell studies
- plain_language
- This study also found protection after targeted MTARC1 loss.
- primary_references
- [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
- tissue_or_cell_type
- Hepatic lipid droplets
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1548–1559
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions · source_derived_draft · unverified_draft
### mo-marc-ko-protection-2026 Global and liver-specific Mtarc1 knockout protected against diet-induced triglyceride accumulation, inflammation and fibrosis. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: This study also found protection after targeted MTARC1 loss. organism: Mus musculus; supporting cell studies tissue_or_cell_type: Hepatic lipid droplets experimental_model: Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions limitations: Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting. exposure: Diet-induced liver disease with gene knockouts/knockdowns and multi-omics evidence_span: {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"} [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
Complete structured claim and evidenceMtarc1 loss post-transcriptionally increased CEPT1 and PEMT, altering lipid-droplet phospholipids; knocking down these enzymes reversed protection.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"}
- experimental_model
- Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions
- exposure
- Diet-induced liver disease with gene knockouts/knockdowns and multi-omics
- limitations
- Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Mus musculus; supporting cell studies
- plain_language
- Changing the droplet surface helped connect the enzyme loss to fat handling.
- primary_references
- [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
- tissue_or_cell_type
- Hepatic lipid droplets
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1561–1572
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions · source_derived_draft · unverified_draft
### mo-marc-lipid-enzymes Mtarc1 loss post-transcriptionally increased CEPT1 and PEMT, altering lipid-droplet phospholipids; knocking down these enzymes reversed protection. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the droplet surface helped connect the enzyme loss to fat handling. organism: Mus musculus; supporting cell studies tissue_or_cell_type: Hepatic lipid droplets experimental_model: Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions limitations: Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting. exposure: Diet-induced liver disease with gene knockouts/knockdowns and multi-omics evidence_span: {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"} [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
Complete structured claim and evidenceThe protection required triglyceride breakdown through lipolysis and lipophagy, tested with Pnpla2 and Lipa inhibition.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"}
- experimental_model
- Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions
- exposure
- Diet-induced liver disease with gene knockouts/knockdowns and multi-omics
- limitations
- Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Mus musculus; supporting cell studies
- plain_language
- Fat had to be broken down for the protective effect to occur.
- primary_references
- [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
- tissue_or_cell_type
- Hepatic lipid droplets
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1574–1585
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions · source_derived_draft · unverified_draft
### mo-marc-lipolysis The protection required triglyceride breakdown through lipolysis and lipophagy, tested with Pnpla2 and Lipa inhibition. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: Fat had to be broken down for the protective effect to occur. organism: Mus musculus; supporting cell studies tissue_or_cell_type: Hepatic lipid droplets experimental_model: Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions limitations: Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting. exposure: Diet-induced liver disease with gene knockouts/knockdowns and multi-omics evidence_span: {"source_cache": "artifacts/molybdenum-research/41641916.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64", "start_char": 0, "end_char": 1681, "text_sha256": "52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64"} [mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. (2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539
Complete structured claim and evidence
What acts on it
The investigators found Marc2 to be the main Marc-family enzyme in mouse liver, with Marc1 contributing relatively little.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/molybdenum-research/38437227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b", "start_char": 0, "end_char": 1333, "text_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b"}
- experimental_model
- Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout
- exposure
- MARC1 variants and mouse global knockout
- limitations
- Human association and mouse intervention are separate. The knockout null result differs from later published mouse knockout protection.
- nutrient_topic
- Molybdenum research collection; topical membership is not evidence of a direct dietary effect. · Molybdenum
- organism
- Human genetics in about 540000 individuals; Mus musculus knockout
- plain_language
- The balance between the two proteins differs across biological settings.
- primary_references
- [mo-p38437227] Divergent role of Mitochondrial Amidoxime Reducing Component 1 (MARC1) in human and mouse. (2024). https://pubmed.ncbi.nlm.nih.gov/38437227/ DOI: 10.1371/journal.pgen.1011179
- tissue_or_cell_type
- Liver phenotypes
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Molybdenum: cofactor assembly, sulfur metabolism and nutrient interactions (2026-09-17) · lines 1522–1533
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout · source_derived_draft · unverified_draft
### mo-marc2-mouse-dominance The investigators found Marc2 to be the main Marc-family enzyme in mouse liver, with Marc1 contributing relatively little. Condition category: machinery_impairment nutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect. plain_language: The balance between the two proteins differs across biological settings. organism: Human genetics in about 540000 individuals; Mus musculus knockout tissue_or_cell_type: Liver phenotypes experimental_model: Multi-ancestry exome association, human protein studies and whole-body mouse Marc1 knockout limitations: Human association and mouse intervention are separate. The knockout null result differs from later published mouse knockout protection. exposure: MARC1 variants and mouse global knockout evidence_span: {"source_cache": "artifacts/molybdenum-research/38437227.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b", "start_char": 0, "end_char": 1333, "text_sha256": "152bcc386bca67c8cd4891d284098784ebbdbf9c507f713f96b996bb3c75bd1b"} [mo-p38437227] Divergent role of Mitochondrial Amidoxime Reducing Component 1 (MARC1) in human and mouse. (2024). https://pubmed.ncbi.nlm.nih.gov/38437227/ DOI: 10.1371/journal.pgen.1011179
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.