Evidence map›Paper›PMID 42631824›Full record

ReviewCell biochemistry and biophysics2026

ABCC6 in Cellular Metabolic Homeostasis: Biochemical Links to Extracellular Nucleotide Signaling, Mitochondrial Stress, and Senescence.

Lingjuan Yang, Fangsicheng Zhang, Yilu Duan, Ying Li, Jiayi Tang, Xinyuan Zhao, Xiaoke Wang

Abstract readReview
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In one paragraph

Review in Cell biochemistry and biophysics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Lingjuan YangInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Fangsicheng ZhangInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Yilu DuanInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Ying LiInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Jiayi TangInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Xinyuan ZhaoInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China.
Xiaoke WangInstitute for Applied Research in Public Health, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong, 226019, China. wxk11628@ntu.edu.cn.ORCID http://orcid.org/0009-0009-9461-7645

Funding

Jiangsu Nantong scientific research project JC2025070Postgraduate Research & Practice Innovation Program of Jiangsu Province KYCX25_3837
6 · The paper itself

Abstract

ABCC6 (ATP-binding cassette subfamily C member 6) was initially identified as the disease gene for pseudoxanthoma elasticum, a disorder marked by ectopic mineralization. Beyond this classical role, emerging evidence supports ABCC6 as a liver-enriched transporter with broader metabolic relevance. ABCC6 promotes hepatocyte ATP (adenosine triphosphate)/ADP (adenosine diphosphate) release and supports ENPP1 (ectonucleotide pyrophosphatase/phosphodiesterase 1)-dependent PPi (inorganic pyrophosphate) generation, thereby maintaining circulating anti-mineralization buffering; downstream AMP (adenosine monophosphate) metabolism may also influence adenosine-related signaling. Although its subcellular localization remains debated, evidence supports predominant basolateral plasma membrane localization, whereas one fractionation study reported enrichment at MAM (mitochondria-associated membranes) that has not been independently validated. ABCC6 deficiency has been associated with altered lipoprotein metabolism, mitochondrial bioenergetic impairment, oxidative stress, senescence-like phenotypes, and context-dependent metabolic susceptibility. These mitochondrial findings are interpreted as ABCC6 deficiency-associated downstream phenotypes rather than as evidence for stable mitochondrial or MAM residence. This review integrates established mineralization biology with emerging metabolic evidence, focusing on the extracellular nucleotide-PPi pathway, downstream adenosine-related signaling, mitochondrial stress, lipid and cholesterol handling, and vascular complications. We also discuss therapeutic strategies aimed at restoring PPi availability, limiting calcification, or recovering ABCC6 expression and function.

Indexed as

ATP-Binding Cassette, Sub-Family C ProteinsCellular SenescenceHomeostasisMitochondriaNucleotidesSignal TransductionAnimalsHumansABCC6 protein, humanATP-Binding Cassette, Sub-Family C ProteinsNucleotidesABCC6Adenosine-Related SignalingAgingExtracellular Nucleotide–PPi PathwayLipid MetabolismMetabolic DiseasesMitochondrial Function

Identifiers

PMID42631824

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.