Calpainopathy, or limb–girdle muscular dystrophy type R1/2A (LGMDR1/2A), is the most prevalent form of LGMD, comprising about 32% of all cases. The disease is caused by mutations in the CAPN3 gene, leading to dysfunction of the corresponding protein–an enzyme critical for muscle fiber cytoskeleton remodeling and protein signaling regulation through selective proteolysis. Clinical manifestations demonstrate significant phenotypic polymorphisms, ranging from oligosymptomatic forms to severe early-onset cases, with the loss of ambulation occurring 10–25 years after disease onset. A characteristic feature is predominantly symmetrical involvement of limb and trunk muscles, leading to early mobility loss, disability, and reduced work capacity. Noninvasive imaging can suggest dystrophic muscle disease but requires differentiation from other myopathies. Confirming the diagnosis involves histological, immunological, and molecular genetic studies to identify calpain-3 activity or CAPN3 gene expression alterations. Currently, no targeted or etiological therapies are available for calpainopathy. Treatment focuses on symptom management, complication prevention, and slowing disease progression. Preclinical research demands the development of an appropriate animal model that displays disease phenotypes mirroring those observed in humans. Preclinical and clinical research are also investigating therapeutic options, including the use of drugs that have proven effective in other myopathies and genome editing via transgenic CAPN3 delivery to restore protein activity. Gene therapy has shown promise in murine models, but safety concerns, particularly systemic toxicity affecting the heart and other organs, remain significant. This review comprehensively analyzes the clinical features, diagnostic approaches, and advancements in modeling and therapeutic development for calpainopathy.

BACKGROUND: About a half a century ago, the concept of physiological regeneration of bone tissue was introduced, which is based on the functioning of basic multicellular units (BMUs). Later, such an approach can also be used to understand the regularities of reparative regeneration. Bone grafting using gene-activated synthetic replacement materials introduces additional features into the reparative process because the material becomes an active participant in the process. Bone grafts sequentially undergo resorption and metabolism and become a matrix on the basis of which the BMUs implement regenerative osteogenesis. AIM: To reveal the function of BMUs in a human bone wound during implantation of a gene-activated osteoplastic material from octacalcium phosphate. MATERIALS AND METHODS: Microfocal computed tomography, histological and immunohistochemical studies, histomorphometry were analyzed and processed statistically. RESULTS: When using an ordinary product and a gene-activated material based on octacalcium phosphate, the bone regenerate was represented by a multi-tissue structure formed by bone beams surrounding non-resorbed fragments of bone replacement products. In the histomorphometric analysis of gene-activated material, the median area of the unresorbed granules was 0.039 [0.013; 0.079] mm2, and the median area of the osteoclasts was 67 [22; 235] cells/mm2. In the group using an ordinary product, the values were 0.029 [0.009; 0.068] mm2 and 15 [0; 79] cells/mm2, respectively. CONCLUSION: BMUs that are in various phases of functional activity (resorption, reversion, formation, and rest) can be detected at the gene-activated material–bone interface. The last phase appears only in cases when the components of the material do not induce osteogenesis.

ОБОСНОВАНИЕ Одним из важных методов лечения химического поражения роговицы является раннее покрытие ее поверхности лоскутом амниотической мембраны. ЦЕЛЬ ИССЛЕДОВАНИЯ Подтвердить эффективность разработанной системы гистологической оценки толщины различных слоев роговицы, с ее помощью определить преимущества раннего покрытия поверхности глаза амниотической мембраной в сочетании с блефарорафией и комплексной консервативной терапией перед аналогичной тактикой без применения амниотической мембраны в эксперименте. МАТЕРИАЛ И МЕТОДЫ Работа выполнена на крысах линии Wistar. Животные (n=32; 64 глаза) были разделены на четыре группы в зависимости от срока выведения из эксперимента. Ожог роговицы формировали при помощи аппликаторов из фильтровальной бумаги, пропитанных 1,0-молярным раствором NaOH. Затем на глазах опытной группы промывали ожоговую поверхность в течение 10 мин, в последующем ее покрывали лоскутом амниотической мембраны и выполняли раннюю блефарорафию. На глазах контрольной группы выполняли аналогичные манипуляции без покрытия амниотической мембраной. В дальнейшем в обеих группах применяли комплексную местную консервативную терапию. При выведении животных из эксперимента оценивали такие клинические признаки, как сохранность шва блефарорафии, реактивное воспаление вспомогательных органов глаза, состояние роговицы (степень эпителизации, обширной неоваскуляризации), субатрофия и тонус глазного яблока. Затем из каждой группы случайным образом выбирали по 2 крысы, у которых удалялись глазные яблоки с последующей гистологической оценкой среза корнеосклерального лоскута. Степень патологических изменений оценивали исходя из объективного измерения толщины стромы роговицы и эпителия в множестве точек среза с последующей статистической оценкой полученных данных. РЕЗУЛЬТАТЫ В группе амниотической мембраны реже выявлялись такие клинические симптомы, как реактивное воспаление вспомогательных органов глаза, субатрофия глазного яблока, а гистологические изменения структуры и толщины эпителия и стромы роговицы были выражены в меньшей степени. ЗАКЛЮЧЕНИЕ Результаты проведенного клинического и гистологического исследования подтверждают преимущества использования в качестве раннего лечения щелочных химических ожогов роговицы глаза покрытие ожоговой поверхности нативной амниотической мембраной.

BACKGROUND: Impaired reparative regeneration leads to insufficient extracellular matrix formation and the development of chronic wounds, necessitating a personalized therapeutic approach. In modern regenerative medicine, biopolymers such as silk proteins serve as the basis for wound dressings and drug delivery systems due to their unique properties. The biocompatibility, modulation of intracellular signaling pathways, and antibacterial activity of spidroin (spider silk protein), fibroin, and sericin (silkworm silk proteins) suggest their potential for wound healing applications. AIM: To evaluate the effects of a spidroin, fibroin, and sericin-based cream on skin regeneration in rats. METHODS: The study included 30 male rats, in which full-thickness excisional skin defects (20 mm in diameter) were created on the back. The animals were divided into three groups: the experimental group, which received daily applications of the test cream, and two control groups—one treated with 5% dexpanthenol and the other left to undergo natural wound healing. Planimetric and histomorphometric analyses, along with clinical blood tests, were performed to assess reparative regeneration and systemic reactive changes. RESULTS: The application of the test cream significantly accelerated wound healing, with complete skin restoration in the experimental group by day 14 compared to the untreated control group. Analysis of inflammatory activity showed moderate granulocytosis and signs of acute posthemorrhagic anemia without pronounced inflammatory alterations in blood parameters. Additionally, immune cell infiltration was lower in the experimental group than in the controls. CONCLUSION: The combination of spider silk proteins (spidroin) and silkworm silk proteins (fibroin and sericin) enhances cell migration, proliferation, and differentiation, promotes extracellular matrix formation, and exerts anti-inflammatory effects without immunogenic properties. These findings support the potential clinical use of this silk protein-based formulation as a therapeutic agent for treating wounds with pathological regeneration.

Background . The diagnosis and management of fungal keratitis remain major challenges in routine ophthalmic practice. This is largely attributable to the severe, treatment-resistant course of the disease and the high risk of recurrence, even when appropriate antifungal therapy is administered. A distinctive feature of keratomycosis is the ability of filamentous fungi to extend beyond the clinically visible margins of the lesion, which may significantly compromise treatment efficacy. The aim . To determine the true extent of mycelial fungal spread within the corneal stroma in keratomycosis. Materials and Methods . The study was performed using an experimental rabbit model of keratitis induced with Fusarium solani isolates. To assess the actual extent of the pathological process, slit-lamp biomicroscopy, anterior segment optical coherence tomography (OCT), and histological examination were employed. Measurements were obtained with consideration of corneal anatomical features. Results . On days 7–9 after keratitis induction, in 9 cases demonstrated a well-defined biomicroscopic appearance consistent with fungal keratitis, with confirmed fungal etiology. Histological examination revealed fungal cells in 17 of 45 sections. A quantitative visual assessment using a corneal microscope and histological examination revealed a difference between these parameters (p = 0.0036), with the median area of proliferation in the corneal stroma being greater than the visually detectable infiltrate. Fungal cells also penetrated the entire corneal thickness in all samples, with detection in the aqueous humor of the anterior chamber. Conclusion . The findings indicate that by day 8 of keratitis progression, the spread of fungal cells along stromal collagen lamellae may exceed the clinically visible lesion by nearly half and extend in depth to involve anterior chamber structures. These growth characteristics of filamentous fungi should be considered when planning the extent of surgical intervention in fungal keratitis.

Skeletal muscle loss resulting from traumatic injury, sarcopenia, and myopathies remains a major clinical challenge due to the limited regenerative capacity of adult muscle tissue. This review systematically examines advanced biomedical therapeutic approaches to restoring muscle mass and function, including gene therapy, microRNA, cell-based strategies, and tissue engineering. Key mechanisms of muscle histogenesis and regeneration are discussed, with emphasis on the roles of satellite cells, growth factors (IGF-1, VEGF), and transcriptional regulators. Preclinical studies demonstrate that viral and non-viral delivery of myogenic factors can enhance muscle repair, reduce fibrosis, and improve functional outcomes. However, translation to clinical practice is hindered by challenges such as immune responses, inadequate reinnervation, and the complexity of replicating native tissue architecture. Emerging strategies combining gene delivery with rehabilitation, immunomodulation, or exosome therapy show synergistic effects. Although clinical trials targeting sarcopenia and muscle defects using anti-myostatin antibodies, stem cell-derived products, and acellular scaffolds have reported modest gains in strength and lean mass, no definitive regenerative therapy has been approved. While significant progress has been made, achieving full structural and functional muscle regeneration will require combinatorial approaches that address vascularization, innervation, and the inflammatory microenvironment.