Muscle-enriched A-type lamin-interacting protein (MLIP) is an emerging protein involved in cellular homeostasis and stress adaptation. Eukaryotic cells regulate various cellular processes, including metabolism, DNA repair, and cell cycle progression, to maintain cellular homeostasis. Disruptions in this homeostasis can lead to diseases such as cancer, characterized by uncontrolled cell growth and division. This review aims to explore for the first time the unique role MLIP may play in cancer development and progression, given its interactions with the PI3K/Akt/mTOR pathway, p53, MAPK9, and FOXO transcription factors, all critical regulators of cellular homeostasis and tumor suppression. We discuss the current understanding of MLIP’s involvement in pro-survival pathways and its potential implications in cancer cells’ metabolic remodeling and dysregulated homeostasis. Additionally, we examine the potential of MLIP as a novel therapeutic target for cancer treatment. This review aims to shed light on MLIP’s potential impact on cancer biology and contribute to developing innovative therapeutic strategies.

Transient Receptor Potential Vanilloid (TRPV) channels represent one of the seven subfamilies of TRP receptors and are widely expressed throughout the human body where they play pivotal roles in various physiological processes. In the gastrointestinal (GI) system, TRPV channels regulate critical functions such as nutrient absorption, motility, and secretions. Beyond maintaining physiological equilibrium, these channels are involved in pain and inflammation, contributing to diverse pathologies. Their central role in the pathophysiology of different digestive system disorders has made TRPV channels a significant focus of research. Moreover, the involvement of TRPV channels in numerous GI cancers has further heightened research interest in the role of these channels. Accordingly, this review elucidates the structural components and intricate signaling pathways of TRPV channels, focusing on the unique characteristics of each family member (TRPV1-6) in GI physiology. Furthermore, we explore the therapeutic potential of targeting these channels to modulate their physiological and pathological roles, highlighting their promise in treating GI disorders. Additionally, we address the challenges associated with their therapeutic application, considering their interactions in different systems, inherent biochemical characteristics, and the alterations required for effective design.

Transient Receptor Potential Vanilloid (TRPV) channels represent one of the seven subfamilies of TRP receptors and are widely expressed throughout the human body where they play pivotal roles in various physiological processes. In the gastrointestinal (GI) system, TRPV channels regulate critical functions such as nutrient absorption, motility, and secretions. Beyond maintaining cellular homeostasis, these channels are involved in pain and inflammation, contributing to diverse pathologies. Their central role in the pathophysiology of different digestive system disorders has made TRPV channels a significant focus of research. Moreover, the involvement of TRPV channels in numerous GI cancers has further heightened research interest in the role of these channels. Accordingly, this review elucidates the structural components and intricate signaling pathways of TRPV channels, focusing on the unique characteristics of each family member (TRPV1–6) in GI physiology. Furthermore, we explore the therapeutic potential of targeting these channels to modulate their physiological and pathological roles, highlighting their promise in treating GI disorders. Additionally, we address the challenges associated with their therapeutic application, considering their interactions in different systems, inherent biochemical characteristics, and the alterations required for effective design.

Diabetes mellitus (DM) is a rapidly growing global health burden and a major driver of infection-related morbidity and mortality. Chronic hyperglycemia disrupts both innate and adaptive immunity through impaired complement activity, dysfunctional dendritic cells and natural killer cells, altered macrophage polarization and efferocytosis, and neutrophil defects including reduced chemotaxis, impaired phagocytosis, and dysregulated NETosis. These immune abnormalities, compounded by endothelial dysfunction and microvascular disease, increase susceptibility to severe and recurrent infections such as urinary tract infections, tuberculosis, pneumonia, skin and soft tissue infections, and invasive fungal diseases. Emerging evidence also supports a bidirectional relationship in which infections may precipitate or aggravate DM via mechanisms including molecular mimicry, β-cell injury, chronic inflammation, and gut microbiota dysbiosis, contributing to insulin resistance and β-cell dysfunction. Recurrent infections and frequent exposure to broad-spectrum antibiotics, together with altered pharmacokinetics, chronic wounds with biofilm formation, and prolonged healthcare exposure, create strong selective pressure for antimicrobial resistance (AMR) in diabetic populations. Using clinical and scientific based evidence, this review explores mechanisms linking DM, infection risk, and AMR, highlighting implications for the diagnosis, therapy, stewardship, and vaccination, as well as outlines key research gaps including improved AMR surveillances stratified by diabetes status and integrated predictive models incorporating glycemic control, host factors, and microbial genomics.

Diabetes mellitus (DM) is a rapidly growing global health burden and a major driver of infection-related morbidity and mortality. Chronic hyperglycemia disrupts both innate and adaptive immunity through impaired complement activity, dysfunctional dendritic cells and natural killer cells, altered macrophage polarization and efferocytosis, and neutrophil defects including reduced chemotaxis, impaired phagocytosis, and dysregulated NETosis. These immune abnormalities, compounded by endothelial dysfunction and microvascular disease, increase susceptibility to severe and recurrent infections such as urinary tract infections, tuberculosis, pneumonia, skin and soft tissue infections, and invasive fungal diseases. Emerging evidence also supports a bidirectional relationship in which infections may precipitate or aggravate DM via mechanisms including molecular mimicry, β-cell injury, chronic inflammation, and gut microbiota dysbiosis, contributing to insulin resistance and β-cell dysfunction. Recurrent infections and frequent exposure to broad-spectrum antibiotics, together with altered pharmacokinetics, chronic wounds with biofilm formation, and prolonged healthcare exposure, create strong selective pressure for antimicrobial resistance (AMR) in diabetic populations. Using clinical and scientific based evidence, this review explores mechanisms linking DM, infection risk, and AMR, highlighting implications for the diagnosis, therapy, stewardship, and vaccination, as well as outlines key research gaps including improved AMR surveillances stratified by diabetes status and integrated predictive models incorporating glycemic control, host factors, and microbial genomics.

Background: Necrotizing fasciitis (NF) is a rare, rapidly progressive soft tissue infection with high morbidity and mortality, if not recognized and treated promptly. While NF typically involves the lower limbs, trunk, or perineum, hand involvement is uncommon, and thumb involvement is exceptionally rare. NF of the hand carries a significant risk of limb loss, with reported amputation rates up to 28%. Early diagnosis, aggressive debridement, and timely reconstruction are essential for functional recovery. Case presentation: We present a 40-year-old male with newly diagnosed type 2 diabetes mellitus who developed severe pain, swelling, and necrosis of the left thumb and hand after drainage of a thumb abscess. Examination revealed extensive necrosis, swelling, crepitus, and loss of thumb function. Imaging showed gas-forming infection, and laboratory studies confirmed systemic inflammation. Emergency debridement and carpal tunnel release were performed, but progression necessitated thumb amputation at the metacarpophalangeal joint and excision of necrotic tissues. Cultures identified Streptococcus constellatus, Streptococcus agalactiae, and anaerobes. Reconstruction was staged with a free anterolateral thigh flap and tendon transfer, followed by a pedicled ulnar artery perforator flap. After a 34-day hospitalization, the patient achieved good healing with viable flaps. Conclusion: Thumb NF is extremely rare but devastating, particularly in diabetic patients with polymicrobial infections. Subtle early signs may mask deep tissue spread. Prompt surgical debridement, multidisciplinary care, and staged reconstruction are critical to optimize outcomes. This case underscores the importance of early recognition, aggressive intervention, and timely reconstruction in preserving hand function in thumb NF.