Evidence map›Paper›PMID 42389811›Full record

ArticleCirculation research2026

Mitochondrial STING Governs Glycolytic Reprogramming in Diabetic Cardiomyopathy.

Shiwu Zhang, Dechao Zhao, Mengyi Wang, Xiaorong Shen, Fan Yang, Zhen Tian, Haining Du, Fanghao Lu, Xueya Zhang, Heyu Chen and 8 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Circulation research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Review
  2. Review
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

18 authors.

Shiwu Zhang *State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.ORCID 0000-0003-3983-4654
Dechao Zhao *Department of Cardiology (D.Z.), First Affiliated Hospital of Harbin Medical University, China.ORCID 0009-0009-3267-0969
Mengyi Wang *State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.ORCID 0000-0002-9348-6876
Xiaorong Shen *State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.
Fan Yang *State Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.ORCID 0000-0003-4676-3778
Zhen TianDepartment of Pathophysiology, School of Basic Medical Sciences (S.Z., M.W., Z.T., H.D., F.L., X.Z., H.C., J.K., W.Z.), Harbin Medical University, China.ORCID 0000-0001-9044-637X
Haining DuState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.
Fanghao LuState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.
Xueya ZhangDepartment of Pathophysiology, School of Basic Medical Sciences (S.Z., M.W., Z.T., H.D., F.L., X.Z., H.C., J.K., W.Z.), Harbin Medical University, China.
Heyu ChenDepartment of Pathophysiology, School of Basic Medical Sciences (S.Z., M.W., Z.T., H.D., F.L., X.Z., H.C., J.K., W.Z.), Harbin Medical University, China.
Jiaxin KangDepartment of Pathophysiology, School of Basic Medical Sciences (S.Z., M.W., Z.T., H.D., F.L., X.Z., H.C., J.K., W.Z.), Harbin Medical University, China.
Mingjie DongCollege of Bioinformatics Science and Technology (M.D.), Harbin Medical University, China.ORCID 0009-0008-7207-008X
Denis V AbramochkinDepartment of Human and Animal Physiology, Biological Faculty, Lomonosov Moscow State University, Russia (D.V.A.).
Huitao FanDepartment of Critical Care Medicine (H.F.), First Affiliated Hospital of Harbin Medical University, China.ORCID 0000-0001-8250-3696
Jinwei TianState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.ORCID 0000-0002-2730-0033
Bo YuState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.ORCID 0000-0002-5955-6332
Shuijie LiState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.ORCID 0000-0003-4538-8996
Weihua ZhangState Key Laboratory of Frigid Zone Cardiovascular Diseases (SKLFZCD) (S.Z., M.W., X.S., F.Y., H.D., F.L., J.T., B.Y., S.L., W.Z.), Harbin Medical University, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundDiabetic cardiomyopathy, a severe complication of diabetes, is marked by mitochondrial dysfunction, metabolic inflammation, and progressive cardiac impairment. Although STING (stimulator of interferon genes) is well recognized as a central mediator of innate immunity, its noncanonical role in metabolic regulation and mitochondrial dynamics in the diabetic heart remains largely unexplored.

methodsTo elucidate the role of STING in diabetic cardiac remodeling, we used single-cell RNA sequencing, echocardiography, and transmission electron microscopy in both genetic (db/db) and chemically induced (high-fat diet [HFD] plus streptozotocin, HFD/streptozotocin) diabetic mouse models. STING knockout mice and primary neonatal mouse cardiomyocytes were used for mechanistic investigations and functional validation. Mitochondrial respiration and glycolytic flux were assessed using Seahorse extracellular flux analysis. Posttranslational modifications of STING, including

resultsExposure to high-palmitate conditions induced mitochondrial DNA leakage, thereby activating the cGAS (cyclic GMP-AMP synthase)-STING (stimulator of interferon genes) signaling pathway in cardiomyocytes. Mechanistically, STING underwent aberrant translocation to mitochondria, where it interacted with the outer membrane protein TOM (translocase of outer mitochondrial membrane) 40 to impair mitochondrial protein import and disrupt mitochondrial homeostasis. In addition, mitochondrial STING functioned as a scaffold to recruit and activate the glycolytic enzyme ENO1, thereby enhancing its enzymatic activity, accelerating glycolytic flux, and promoting lactate accumulation in diabetic cardiac tissues. Notably, diabetes-associated depletion of endogenous hydrogen sulfide reduced

conclusionsThese findings identify STING as a spatial immunometabolic modulator that bridges mitochondrial dysfunction with metabolic imbalance in diabetic cardiomyopathy. Enhancing STING

Indexed as

Diabetic CardiomyopathiesGlycolysisMembrane ProteinsMitochondria, HeartMyocytes, CardiacAnimalsCells, CulturedcGAS-STING Signaling PathwayCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseDiabetes Mellitus, ExperimentalMaleMetabolic ReprogrammingMiceMice, Inbred C57BLMice, KnockoutSTING ProteincGAS protein, mouseCyclic Guanosine Monophosphate-Adenosine Monophosphate SynthaseMembrane ProteinsSting1 protein, mouseSTING Proteindiabetic cardiomyopathiesinflammationmetabolismmitochondriastreptozotocin

Identifiers

PMID42389811
PMCPMC13418885

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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 OpenQuestion graph.