Diabetic cardiomyopathy (DCM) represents a complex and debilitating complication arising from the intricate interplay between diabetes mellitus and cardiovascular dysfunction [1]. As the prevalence of diabetes continues to surge globally, the burden of DCM has become increasingly pronounced, necessitating innovative approaches for its therapeutic management [2]. Among the diverse pathophysiological mechanisms implicated in DCM, dysregulation of autophagy has emerged as a focal point of research, offering a unique avenue for targeted interventions [3]. The intricate pathophysiology of DCM involves a cascade of events, including oxidative stress, inflammation, and mitochondrial dysfunction, collectively contributing to cardiac remodelling and dysfunction [4], [5]. The bidirectional relationship between diabetes-induced stressors and autophagy dysregulation establishes a compelling rationale for targeting this process in the quest for therapeutic solutions [6] (Fig. 1).

Noncoding RNAs, once dismissed as "junk" genetic material, have emerged as master regulators of gene expression and key players in cellular homeostasis. miRNAs, lncRNAs, and circRNAs constitute diverse classes of ncRNAs with the ability to modulate a myriad of biological processes [7]. Recent research has unveiled their intricate involvement in autophagy regulation, prompting a paradigm shift in our understanding of the molecular underpinnings of cellular dynamics [8]. MicroRNAs, short ncRNAs with post-transcriptional regulatory functions, have emerged as influential mediators in the autophagy-diabetic Cardiomyopathy axis [9]. Specific miRNAs such as miR-30, miR-133, and miR-155 have been implicated in modulating autophagy, exerting both protective and detrimental effects on cardiac function [10]. Long noncoding RNAs, with their diverse structural and functional properties, have also entered the spotlight as orchestrators of autophagic harmony in the diabetic cardiomyopathic milieu. Examples such as H19, MALAT1, and NEAT1 have been identified as key players in modulating autophagy and cardiac function [11], [12]. Circular RNAs, characterized by their closed-loop structure, have emerged as promising candidates for circumventing autophagic imbalance in diabetic cardiomyopathy [13]. CircRNAs such as circRNA_010567 and circHIPK3 have been implicated in modulating autophagy-associated signaling pathways, offering novel insights into potential therapeutic targets [14]. Experimental and preclinical studies have demonstrated the feasibility of manipulating specific ncRNAs to restore autophagic homeostasis, mitigating cardiac dysfunction in diabetic models [15]. As we delve deeper into the molecular intricacies, the prospect of designing precision therapies targeting ncRNAs brings us closer to realizing effective interventions for diabetic cardiomyopathy [16], [17]. The convergence of diabetes-induced stressors and perturbed autophagy sets the stage for innovative therapeutic approaches [18]. Noncoding RNAs, with their regulatory prowess, stand as promising candidates for targeted interventions, offering hope for a future where the burdens of diabetic cardiomyopathy can be alleviated through precision medicine strategies [19], [20]. In this comprehensive review, we delve into the intricate connections between autophagy dysregulation and diabetic cardiomyopathy, exploring the unprecedented potential of noncoding RNAs (ncRNAs) as precise therapeutic targets.