The role of miR-128 and MDFI in cardiac hypertrophy and heart failure: Mechanistic.

Heart failure (HF) prognosis depends on various regulatory factors; microRNA-128 (miR-128) is identified as a regulator of cardiac fibrosis, contributing to HF. MyoD family inhibitor (MDFI), which is reported to be related with Wnt/ß-catenin pathway, is supposed to be regulated by miR-128. This study investigates the interaction between miR-128 and MDFI in cardiomyocyte development and elucidates its role in heart injury. Gene expression profiling assessed miR-128's effect on MDFI expression in HF using qPCR and Western blot analysis. Luciferase assays studied the direct interaction between miR-128 and MDFI. MTT, transwell, and immunohistochemistry evaluated the effects of miR-128 and MDFI on myocardial cells in mice HF. Genescan and luciferase assays validated the interaction between miR-128 and MDFI sequences. miR-128 mimics significantly reduced MDFI expression at mRNA and protein levels with decrease rate of 55%. Overexpression of miR-128 promoted apoptosis with the increase rate 65% and attenuated cardiomyocyte proliferation, while MDFI upregulation significantly enhanced proliferation. Elevated miR-128 levels upregulated Wnt1 and ß-catenin expression, whereas increased MDFI levels inhibited these expressions. Histological analysis with haematoxylin and eosin staining revealed that miR-128 absorption reduced MDFI expression, hindering cell proliferation and cardiac repair, with echocardiography showing corresponding improvements in cardiac function. Our findings suggest miR-128 interacts with MDFI, playing a crucial role in HF management by modulating the Wnt1/ß-catenin pathway. Suppression of miR-128 could promote cardiomyocyte proliferation, highlighting the potential value of the miR-128/MDFI interplay in HF treatment.

Correction of Cicatricial Lower Eyelid Retraction and Entropion With Combined Scar Release, Hard Palate Graft, and Lateral Canthal Suspension.

OBJECTIVE: This study aimed to evaluate the outcome of a technique-combined scar release, hard palate spacer graft with the recession of the lower eyelid retractors, lateral canthal suspension in the repair of cicatricial lower eyelid retraction, and entropion. METHODS: Records of 12 patients with cicatricial lower eyelid retraction and entropion who underwent the surgery from January 2019 to August 2021 were reviewed. Surgical techniques include the following procedures: release of scar, hard palate graft with recession of the lower eyelid retractors, and lateral canthal tightening to strengthen the support of the lower eyelid. The follow-up period was at least 12 months. Postoperative outcomes were evaluated by the improvement of lower eyelid retraction, resolution of eyelid entropion, and complications. RESULTS: All patients showed resolution in lower lid entropion, and lower eyelid retraction was significantly improved with a mean elevation of 2.93±0.82 mm. None of the patients had severe complications postoperatively, and both ocular surface symptoms and cosmetic appearance were significantly improved. CONCLUSIONS: The technique achieves long-term stable outcomes in cicatricial lower lid retraction and entropion repair with a low morbidity rate.