Depression and obesity are amongst the most serious global health challenges. Each of them is associated with high morbidity, chronicity, and socioeconomic burden. Increasing evidence suggests that these conditions are not merely comorbid but share convergent biological pathways (e.g., hypothalamic–pituitary–adrenal axis dysregulation, chronic inflammation, gut dysbiosis, and mitochondrial dysfunction). All these components contribute together to the development and persistence of depressive symptoms as well as to an increase in adiposity. Within this framework, adipose tissue has emerged as an essential endocrine organ that has a deep impact on neuroimmune signalling and mood regulation through its secreted molecules, such as leptin, adiponectin, resistin, omentin, apelin, chemerin, and visfatin. The current management of depression involves a comprehensive, multidisciplinary approach that includes pharmacological treatment and psychotherapeutic support, alongside lifestyle changes. Here we highlight the molecular crosstalk between adipose tissue and the brain, summarising the evidence of adipokines’ dysregulation role in connecting metabolic dysfunction to depressive neurobiology. By integrating metabolic, immunological, and neuroendocrine perspectives, this narrative review underscores the need to reconceptualise depression as an immunometabolic disorder. Understanding adipokine-mediated pathways may reveal new biomarkers and therapeutic targets, fostering interdisciplinary approaches. This would allow for the development of new treatment strategies, which include recombinant adipokines, anti-inflammatory agents, and microbial modulation. These new strategies might provide a significant benefit in selected patients, in addition to conventional antidepressants.

Background: Wearable electrocardiography (ECG) devices such as smartwatches offer a novel means for detecting cardiac arrhythmias, particularly atrial fibrillation (AF), and ST-segment abnormalities. Their role in complementing or replacing traditional ECG methods is being increasingly investigated. Objective: To evaluate the diagnostic performance (sensitivity, specificity) of wearable ECG devices in detecting AF and ST-segment changes, compared to 12-lead ECG as the gold standard. Methods: A systematic search was performed in PubMed, Scopus, and additionally, the SpringerLink platform was consulted up to June 2025, targeting open-access, English-language clinical studies from the last five years. Inclusion criteria: adult population, use of a wearable ECG device, 12-lead ECG comparator, and diagnostic accuracy reporting. Out of 145 records, 5 studies met the inclusion criteria. The systematic review protocol was not prospectively registered in PROSPERO due to the limited number of available studies and the exploratory nature of the topic, which focused on the most recent clinical evaluations of wearable ECG devices. However, the review strictly adhered to the PRISMA 2020 guidelines for systematic reviews to ensure methodological transparency and reproducibility. Results: Five studies encompassing a total of 1133 participants were incorporated into the analysis. Devices evaluated included Apple Watch (Series 4–6), KardiaMobile 6L, FibriCheck, Preventicus, and HUAMI dynamic ECG. Sensitivity ranged from 83% to 100%, and specificity from 79% to 100%. Algorithm improvements and repeated measurements significantly reduced inconclusive recordings. Multichannel ECG methods using smartwatches showed high agreement with 12-lead ECG in ST-elevation myocardial infarction detection. Conclusions: Wearable ECG devices demonstrate high diagnostic performance for AF and ST-segment abnormalities, especially in supervised environments. However, inconclusive recordings and algorithm limitations remain barriers to widespread clinical use. Real-world validation and algorithm refinement are needed for broader adoption.

Perirenal adipose tissue (PRAT) has emerged as a clinically relevant endocrine organ connecting obesity to cardiovascular disease (CVD), chronic kidney disease, and certain malignancies. Its unique anatomical location, surrounding the kidneys, accounts for PRAT’s role in altering intrarenal haemodynamics and hydrostatic pressure. Accordingly, PRAT’s expansion is associated with the activation of the renin–angiotensin–aldosterone system (RAAS), further increasing blood pressure. Adipokine dysregulation, together with overexpression of miR-24-3p, miR-155, miR-146a, and miR-21 in PRAT, modulates inflammation and oxidative stress, leading to endothelial dysfunction and increased risk of atherosclerosis and hypertension in obesity. Imaging assessment of PRAT thickness through computed tomography, magnetic resonance, or ultrasound has also emerged as a complementary measure for the evaluation of CVD risk. Potential therapeutic strategies targeting PRAT include lifestyle interventions, antidiabetic agents, RAAS inhibitors, adipose tissue browning agents, NOD-like receptor protein 3 (NLRP3) inflammasome inhibitors, peroxisome proliferator-activated receptor gamma (PPARγ) agonists, and surgery. Currently, novel therapeutic interventions targeting PRAT activity in CVD, such as senotherapeutic strategies, bioengineering approaches aimed at enhancing adipose-derived mesenchymal stem cell (ADMSC) function, gut microbiota modulation, and colchicine and bone morphogenetic protein 4 (BMP4) administration, are also being explored. In light of these findings, PRAT’s clinical relevance extends beyond its energy storage role, highlighting it as a metabolically active fat depot. Its assessment and therapeutic modulation may complement existing cardiovascular prevention strategies, particularly in patients with obesity.