This PubMed record corresponds to an article in Circulation Research with the title “Methylmalonate Overload Despite Glycemic Control Drives Diabetic Heart Damage.” The journal citation listed in the record is Circ Res. 2026 Aug 28;139(6):e327192, with doi 10.1161/CIRCRESAHA.125.327192 and an electronic publication date of 2026 Jul 29.
The PubMed entry provides the official bibliographic metadata required to locate the study in journal databases. A link to the publisher-hosted full text (Atypon) is included in the PubMed record.
The article lists a large collaborative author group led by Shanjie Wang, Miao Yan, and Yiying Zhang (noted as equal contributors). Many coauthors are affiliated with the Department of Cardiology, Second Affiliated Hospital of Harbin Medical University and The Key Laboratory of Myocardial Ischemia, Chinese Ministry of Education and SKLFZCD. Additional affiliations include the Department of Epidemiology and Biostatistics at Jiamusi University, the Department of Cardiology at Xijing Hospital of Fourth Military Medical University, the Department of Health Research Methods, Evidence, and Impact at McMaster University, and other institutions.
The PubMed record provides institutional attributions for most listed authors, but the supplied content stops within the author/affiliation section and does not include the full-body text or abstract.
The title identifies the central focus as the role of methylmalonate overload in promoting diabetic heart damage even when glycemic control is achieved. From that title one can infer the study addresses a metabolic contributor to cardiac injury in diabetes that may be independent of blood-glucose levels.
Key clinical and translational terms derived from the record include: methylmalonate, diabetic cardiomyopathy/heart damage, and glycemic control. These terms point to an intersection of metabolic biochemistry and cardiometabolic disease relevant to pharmacology and cardiovascular research.
The PubMed entry contains a “Full text links” section and an Atypon publisher link. Readers seeking full methodological details, experimental design, cohort descriptions, statistical analyses, numeric results, figures, and authors’ interpretations should use the provided full-text link or consult institutional access to Circulation Research.
The source material supplied for this rewrite is the PubMed landing page content and metadata only. The following critical items were not present in the supplied source text and therefore are not reported here:
Because these critical elements are missing from the provided source content, no attempt is made to infer or restate findings beyond what the title and bibliographic metadata assert.
Based strictly on the article title and available metadata, the principal clinical implication is that accumulation or overload of methylmalonate may contribute to cardiac injury in people with diabetes despite achieving glycemic control. This raises the translational question of whether metabolic pathways beyond glucose regulation—such as those involving methylmalonate metabolism—could be therapeutic targets to reduce diabetic cardiac injury.
However, the PubMed record supplied here does not include the data required to evaluate the strength of evidence, the clinical relevance, or whether findings were derived from animal experiments, mechanistic cellular studies, observational human cohorts, or interventional trials. Therefore, any clinical interpretation must be deferred until the full article is reviewed.
To evaluate methods, results, and clinical recommendations, consult the publisher link provided in the PubMed entry (Atypon / Circulation Research). Use institutional access, interlibrary loan, or contact the corresponding author(s) if access is restricted. The PubMed record’s DOI (10.1161/CIRCRESAHA.125.327192) and the citation (Circ Res. 2026 Aug 28;139(6):e327192) can be used to locate the article in journal databases.
Note: This rewritten summary preserves the metadata and title-derived focus from the supplied PubMed record. Specific experimental findings, numerical results, and authors’ conclusions were not included in the source material provided and therefore are not reported here. For evidence-based clinical application, consult the full text.