Metabolic dysfunction-associated steatotic liver disease (MASLD), the most common chronic liver disorder worldwide, results from multidimensional network dysregulation involving lipid metabolism imbalance, insulin resistance, oxidative stress, chronic inflammation, and gut-liver axis disruption. Silent information regulator 1 (SIRT1), an NAD+-dependent deacetylase, functions as a central regulator of metabolic homeostasis and a key mediator in immune microenvironment remodeling and inter-organ communication. This review systematically describes the multi-target mechanisms of SIRT1 in MASLD pathogenesis through its regulation of critical factors, including peroxisome proliferator-activated receptor gamma coactivator 1-α, Forkhead Box O, and nuclear factor kappa-light-chain-enhancer of activated B cells, which govern hepatocyte lipid remodeling, mitochondrial quality control, autophagy–endoplasmic reticulum stress balance, and Kupffer cell/T cell polarization. This work introduces, for the first time, the concept that SIRT1 mediates systemic regulation of MASLD via coordinated “metabolism–inflammation–organ axis” interactions. Recent studies indicate that natural compounds (e.g., resveratrol, curcumin) improve gut-liver barrier function through microbiota–SIRT1 interactions, while synthetic activators (SRT1720) and NAD+ precursors (NMN) enhance hepatocyte antioxidant capacity and fatty acid β-oxidation. This innovative analysis highlights the spatiotemporal specificity of various SIRT1 activators, emphasizing that tissue-selective delivery and dynamic dosage optimization are crucial for overcoming clinical translation challenges. By integrating mechanistic and translational insights, this review provides a novel foundation for precision intervention strategies targeting SIRT1 network reprogramming.

Type 2 diabetes (T2D) is a metabolic disorder characterized by insulin resistance (IR), inflammation, and dysregulation in glucose metabolism. The disease is spreading globally, partly due to aging, which can damage the immune system and speed up the progression of the metabolic disorder. This review primarily delves into the triggers for T2D within the framework of the ominous octet, which emphasizes 8 principal factors under the “ominous octet” framework that contribute to high blood glucose and associated metabolic disorders. The article studies the interplay of hyperinsulinemia, mitochondrial dysfunction (MD), and endoplasmic reticulum (ER) stress with immune aging in driving disease progression affecting each component of the octet. MD and ER stress can result in defects in insulin signaling, ultimately leading to β-cell death. Chronic inflammation associated with aging, also known as inflammaging, especially affects older adults by worsening IR and glucose regulation, which creates a continuous sequence of metabolic problems. Thus, the “ominous octet” framework provides fundamental knowledge to develop personalized treatment approaches that target metabolic dysfunction together with ER stress, MD, and immune system imbalances. These strategies show promising potential to improve treatments for T2D and may lead to better health outcomes for older adults dealing with this condition.

The proto-oncogene c-Fos is known as a reliable marker of cell activation, which is immediately induced after a new stimulus in specific brain regions, depending on the nature of the stimulus applied. However, the expression of c-Fos is increased in Alzheimer’s disease (AD) and contributes to amyloid β-peptide-induced neurotoxicity. This review attempted to focus on the role of c-Fos in learning and memory in both healthy brain and AD, emphasizing on possible mechanisms. Comparing the available findings, regarding learning and memory, c-Fos expression leads to memory formation through ERK (extracellular signal-regulated kinase)/CREB (cAMP response element-binding protein) and long-term potentiation, while it is down regulated after the repetition and habituation of stimuli. However, its overexpression in neurons and glia of AD, contributes to cognitive deficits and neuronal loss, which represents a defect in its ability to habituate to repeated stimuli. Also, expression pattern in glial is associated with constitutive CREB activation following increasing amyloid beta (Aβ), activation transcription factor (ATF3), and cytochrome c in apoptosis pathways. Thus, two contradictory roles of c-Fos in the healthy brain and AD, reveal more complexity in c-Fos up and down stream signaling pathways, bioavailability, and sensitivity. Future studies focusing on c-Fos modulation, might offer promising strategies to mitigate cognitive decline in AD.

Chronic subdural hematoma (CSDH) is a common disease in neurosurgery, with epidemiological characteristics showing an overall annual incidence of 1.7–20.6 per 100,000 people and a higher prevalence in the elderly. However, despite the increased disease burden, there have been limited breakthroughs in treatment options over the past 20 years. A significant gap exists in our understanding of the exact pathophysiological mechanism of CSDH, leading to a lack of specific clinical treatment options based on a clear pathological mechanism. Current research suggests that the development of CSDH involves dual mechanisms of trauma and inflammation, and that these pathologic processes together promote pathological changes such as angiogenesis, inflammatory response, and neovascularization. Therapies for CSDH encompass both surgical (e.g., twist-drill drainage, burr-hole drainage, craniotomy) and non-surgical approaches (e.g., clinical observation, medication, intracranial pressure monitoring, anticoagulation). Meanwhile, middle meningeal artery embolization, as an emerging minimally invasive interventional technique, has shown good prospects for clinical application. This review aims to bridge the gap between current treatment options and the need for effective strategies by providing a comprehensive summary of the epidemiological trends, pathophysiological advances, and optimization of therapeutic strategies for CSDH.

Breast cancer remains one of the leading causes of cancer-related deaths worldwide. Early detection of breast cancer significantly improves outcomes and survival rates, minimizing treatments. Imaging techniques are critical in identifying abnormalities and diagnosing breast cancer at its earliest stages, often before clinical symptoms emerge. Mammography remains standard for screening in average-risk women, while supplementary methods like ultrasound, magnetic resonance imaging, and tomosynthesis enhance detection rates, particularly in women with dense breasts or those at high risk. Given that certain factors, such as family history, age, genetic mutations, and breast density, affect the risk of developing breast cancer, some women may benefit from earlier or more frequent screenings. Personalized screening protocols are becoming more common, tailoring the type and frequency of imaging to the individual’s risk profile. Newer technologies, such as molecular breast imaging and contrast-enhanced mammography show promise but require further validation for widespread use. In conclusion, imaging techniques including mammography, ultrasound, magnetic resonance imaging, and newer technologies like three-dimensional mammography and molecular breast imaging are essential tools in the early detection of breast cancer, leading to better outcomes for patients. This literature review provides an overview of current breast cancer imaging methods, their role in early diagnosis, and their effectiveness and limitations.

FMS-like tyrosine kinase 3 (FLT3) mutations are among the most common genetic alterations in acute myeloid leukemia (AML) and play a pivotal role in leukemogenesis. The two primary mutation types, internal tandem duplications (ITDs) and tyrosine kinase domain point mutations, serve as key prognostic markers and therapeutic targets. Advances in next-generation sequencing (NGS) have revolutionized FLT3 mutation detection by providing precise insights into mutation architecture, enhancing risk stratification, and enabling personalized treatment strategies. Additionally, these advancements have facilitated molecular minimal residual disease (MRD) testing, which is instrumental in guiding post-remission management. This review summarizes the molecular characteristics, diagnostic approaches, and therapeutic implications of FLT3 mutations in hematologic malignancies.

A narrative review of the current literature on FLT3 mutations was conducted, incorporating data from original research articles, clinical trials, and recent reviews. Relevant studies were identified through a PubMed literature search and manually curated.

FLT3 mutations are detected in approximately 30% of AML cases and occur at lower frequencies in myelodysplastic syndromes, chronic myelomonocytic leukemia, acute lymphoblastic leukemia, and mixed phenotype acute leukemia. NGS enables comprehensive mutation profiling, revealing rare variants and subclonal complexity while supporting MRD detection with high analytic sensitivity. FLT3-ITD-based MRD positivity is strongly associated with relapse and poor survival in AML. Clinical trial data support FLT3 inhibitors, including midostaurin, gilteritinib, and quizartinib, in FLT3-mutated AML. Additionally, MRD-guided therapy and combination treatment strategies are promising approaches to overcoming resistance.

FLT3 mutations play a central role in the pathogenesis and treatment of AML and related malignancies. NGS-based testing and MRD monitoring transform clinical decision-making by refining risk stratification and enabling personalized therapeutic interventions. Establishing standardized testing protocols and the broader integration of FLT3-targeted therapies will be essential for optimizing patient outcomes.

Thrombocytopenia in cirrhosis presents significant challenges in clinical practice. To help clinicians rapidly understand and standardize the diagnosis and treatment of this condition, the Liver Fibrosis, Cirrhosis, and Portal Hypertension Group under the Chinese Society of Hepatology, Chinese Medical Association, convened experts across relevant fields to formulate the Expert Consensus for the Management of Thrombocytopenia in Cirrhosis. This consensus aimed to provide evidence-based guidance for clinical diagnosis and treatment.

Type 1 diabetes (T1D) develops when the immune system targets and destroys pancreatic β-cells responsible for insulin production, ultimately resulting in reduced insulin levels. Islet transplantation has garnered significant attention as a potential treatment, but it presents numerous challenges that hinder its effectiveness for T1D patients. A primary issue is the immune system’s tendency to reject transplanted islets, leading to a gradual decline in their functionality. Furthermore, many individuals remain reliant on additional insulin therapy. These challenges are exacerbated by the global shortage of organ donors, which limits the availability of pancreata for transplantation. This review outlines several innovative strategies to regenerate insulin-producing β-cells for the treatment of T1D, with a primary focus on pancreatic progenitor and stem cells. The strategy of converting non-β cells, particularly pancreatic α-cells, into functional β-cells continues to show promise. Moreover, α-cells, which are less vulnerable to autoimmune attacks, present a distinct opportunity for β-cell regeneration in individuals with T1D. While the use of progenitor or stem cells for β-cell regeneration appears encouraging, various hurdles, such as immune rejection, suboptimal differentiation, and other challenges, still impede the implementation of this strategy. Nonetheless, this approach may ultimately pave the way for long-lasting treatment and potential cures for T1D.

Acute liver failure (ALF) is a disorder with various etiologies. Although the causes leading to this disruptive condition are well documented in published ALF cohorts, there is significant concern among patients who experience ALF with indeterminate causes, an issue requiring thorough analysis. This review aimed to analyze cohort studies on ALF with a focus on unknown causes leading to classification as indeterminate ALF. The analysis revealed that, among 67 worldwide adult and pediatric ALF cohorts, indeterminate causes of ALF ranged from 2% to 100%, with an average of 30%. Among the 13 pediatric ALF cohorts, the corresponding range was 22% to 100%, with an average of 47%, while among the 55 adult ALF cohorts, the range was 2% to 78%, with an average of 26%. The percentage values were higher in pediatric cohorts due to the higher incidence of rare genetic causes compared to adult patients. Notably, higher rates of indeterminate causes were found in cohorts studied before the availability of diagnostic serologic screening parameters and polymerase chain reaction techniques for various hepatitis virus infections. Patients with indeterminate ALF may not have received a specific treatment that, if effective, could have helped prevent liver transplantation. It is concluded that, in future cases, all efforts must be undertaken to clearly establish the cause of severe liver injury, enabling effective therapy when available and helping reduce the risk of progression to ALF and the need for liver transplantation.

Gastrointestinal (GI) health is essential for maintaining systemic balance, influencing digestion, immunity, and neuroendocrine signaling. However, GI disorders such as irritable bowel syndrome, inflammatory bowel disease, gastroesophageal reflux disease, peptic ulcers, and constipation are increasingly prevalent, significantly affecting global health and healthcare economics. Although conventional pharmacological treatments offer symptomatic relief, their long-term use is often associated with adverse effects, resistance, and limited efficacy, prompting a shift toward alternative and complementary therapies. Traditional systems of medicine, such as Ayurveda, Traditional Chinese Medicine, Unani, and Siddha, emphasize holistic approaches, including herbal formulations that target underlying causes rather than just symptoms. This review provides a comprehensive analysis of the role of natural products and traditional herbals in GI health. It discusses key bioactive constituents, flavonoids, alkaloids, terpenoids, and polyphenols, known for their anti-inflammatory, antimicrobial, gastroprotective, and prebiotic properties. Widely used herbal remedies such as Triphala, licorice root, peppermint oil, turmeric, and psyllium are highlighted for their proven therapeutic actions. Additionally, the review documents more than 300 medicinal plants traditionally used in diverse cultures worldwide for managing GI conditions, based on ethnopharmacological evidence. While the therapeutic promise is substantial, challenges such as formulation standardization, herb-drug interactions, and limited clinical data remain. The review underscores the need for integrating traditional wisdom with modern scientific validation, offering a path forward for safe, effective, and personalized GI healthcare.