Background: Tracheal grafts have been investigated for over a century, aiming to replace various lesions. However, tracheal reconstruction surgery remains a challenge, primarily due to anatomical considerations, intraoperative airway management, the technical complexity of reconstruction, and the potential postoperative morbidity and mortality. Due to research development, the amniotic membrane (AM) and Wharton’s Jelly (WJ) arise as alternatives within the new set of therapeutic alternatives. These structures hold significant therapeutic potential for tracheal defects. This study analyzed the capacity of tracheal tissue regeneration after 60 days of decellularized WJ and AM implantation in rabbits submitted to conventional tracheostomy. Methods: An in vivo experimental study was carried out using thirty rabbits separated into three groups (Control, AM, and WJ) (n = 10). The analyses were performed 60 days after surgery through immunohistochemistry. Results: Different immunomarkers related to scar regeneration, such as aggrecan, TGF-β1, and α-SMA, were analyzed. However, they highlighted no significant difference between the groups. Collagen type I, III, and Aggrecan also showed no significant difference between the groups. Conclusions: Both scaffolds appeared to be excellent frameworks for tissue engineering, presenting biocompatibility and a desirable microenvironment for cell survival; however, they did not display histopathological benefits in trachea tissue regeneration.

This study assessed the impact of implanting mononuclear stem cells and Wharton’s Jelly (WJ), either separately or together, on left ventricular dysfunction following myocardial infarction in Wistar rats. Functional and histopathological parameters were analyzed, and a rat model of left anterior descending coronary artery ligation was used. Treatments included an intramyocardial injection of 0.9% sodium chloride (control, n = 14), decellularized WJ (n = 12), bone marrow-derived mononuclear cells (BMMC) (n = 12), and bone marrow-derived mononuclear cells (BMMC) combined with WJ (n = 15). Echocardiography assessed the left ventricular function and ejection fraction over four weeks. Histological and immunohistochemical analyses with anti-factor VIII evaluated angiogenesis and collagen types I and III. The results showed no statistically significant effect on ventricular remodeling 30 days post-acute myocardial infarction (AMI). Moreover, the infarct area was significantly smaller in the BMMC + WJ group compared to the control group, suggesting a potential benefit in reducing myocardial scarring. BMMC + WJ therapy demonstrated potential for functional improvement and infarct size reduction 30 days post-infarction. Further studies are needed to confirm its therapeutic benefits.

Background/Objectives: Acute myocardial infarction (AMI) remains a major cause of global morbidity and mortality and is a leading factor in the development of heart failure. This study investigated the regenerative potential of decellularized human amniotic membrane (HAM) and Wharton’s jelly (WJ) in a rat model of left ventricular dysfunction induced by acute myocardial infarction (AMI). Methods: Twenty-three rats underwent left anterior descending coronary artery ligation and were randomized into three groups: control (saline), WJ (decellularized WJ), and HAM (decellularized HAM). Results: After 30 days, echocardiographic, histopathological, and immunohistochemical assessments were performed. No significant differences in ventricular function were observed among groups. However, the HAM-treated group showed a significant reduction in myocardial fibrosis compared with the control (p = 0.009), suggesting attenuation of post-infarction remodeling. Despite the absence of measurable functional recovery, HAM demonstrated potential to promote more favorable tissue organization. Study limitations include the lack of a sham-operated group, short follow-up period, and absence of quantitative decellularization validation. Conclusions: Overall, the results indicate that decellularized HAM may act as a structural modulator of myocardial remodeling, warranting further studies with longer follow-up and combination approaches, such as cell-based or growth factor-enhanced therapies.

Introduction. Acute myocardial infarction is caused by a lack of oxygen supply to the myocardium, which results in the loss of cardiomyocytes and replacement by fibrotic scar tissue, and this event is related to the development of heart failure. Regenerative medicine has emerged as an option to increase the effectiveness of treatment for severe cases of heart failure. Objectives. To evaluate the potential for myocardial regeneration after acute myocardial infarction, using biomaterial made from Mononuclear Stem Cells and Human Amniotic Membrane. Materials and Methods. For the study, 120 Wistar rats were submitted to experimental acute myocardial infarction. On the 7th day, rats with an ejection fraction of < 50% on echocardiography were randomized into four groups: 1- control; 2- stem cells; 3- amniotic membrane; 4- amniotic membrane associated with stem cells. On the 30th day, the surviving animals underwent echocardiography and were then euthanized. Results. There was a reduction in systolic and diastolic volume in the amniotic membrane associated with stem cells group. Histological analysis showed that the animals in this group had less fibrosis and a lower percentage of type I collagen. Conclusion. The animals in the stem cell-associated amniotic membrane group had reduced ventricular volumes and less fibrosis.