Diabetic Cardiomyopathy: An Update of Mechanisms Contributing to This Clinical Entity.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing pathophysiological mechanisms without systematic review or original data
PubMed 29449364 · doi:10.1161/CIRCRESAHA.117.311586
What was done
Narrative review summarizing the clinical progression, pathophysiological features, and cellular and molecular mechanisms implicated in diabetic cardiomyopathy (defined as myocardial dysfunction in diabetes mellitus in the absence of coronary artery disease, valvular disease, or other conventional cardiovascular risk factors), along with mechanistically based therapeutic strategies.
What was found
The abstract provides no quantitative data or numerical findings. It qualitatively outlines the clinical progression of diabetic cardiomyopathy from early myocardial fibrosis, remodeling, and diastolic dysfunction to subsequent systolic dysfunction and overt heart failure. It identifies key contributing mechanisms including impaired cardiac insulin signaling, mitochondrial dysfunction, oxidative stress, reduced nitric oxide bioavailability, advanced glycation end-product accumulation, altered calcium handling, inflammation, renin-angiotensin-aldosterone system activation, cardiac autonomic neuropathy, endoplasmic reticulum stress, microvascular dysfunction, and altered signaling via AMPK, PPARs, protein kinase C, microRNAs, and exosomes.
Why it matters
Provides a comprehensive overview of the complex, multifactorial molecular and metabolic drivers of diabetes-associated heart failure, helping frame targets for prevention and mechanistic therapies.
Limits
This is a narrative review with no primary empirical data, quantitative synthesis, or reported systematic search methodology. Specific effect sizes, diagnostic criteria performance, and clinical trial outcomes are not reported in the abstract.
Cited by
- supports Chronically elevated blood glucose levels react with collagen in cardiac tissue, causing stiffening of the myocardium and pericardium and lowering cardiac compliance.