Translational Health Reports

Abstract Background: Coronary Heart Disease (CHD) is a widespread health challenge characterized by intricate pathophysiological mechanisms such as chronic inflammation, endothelial impairment, and metabolic irregularities. Exercise-focused Cardiac Rehabilitation (CR) is a key element of secondary prevention, known to decrease mortality and improve health outcomes. Examining its impact on a diverse range of biomarkers offers deeper insight into the biological mechanisms behind these benefits.
Objective: This systematic review consolidates current research on the effects of structured exercise training within CR on biomarkers related to critical pathological areas in CHD patients, including inflammation, lipid metabolism, vascular function, myocardial stress, and metabolic health.
Methods: A systematic search of PubMed, Scopus, and the Cochrane Central Register of Controlled Trials was conducted from January 2000 to May 2024. Randomized controlled trials, meta-analyses, and prospective cohort studies evaluating the impact of exercise-based CR on biomarkers in adults with confirmed CHD were included.
Results: Analysis of 40 high-quality studies shows that exercise-based CR consistently produces beneficial changes across multiple biomarker pathways. Notable findings include significant decreases in high-sensitivity C-reactive protein (median reduction of 32%), interleukin-6, and tumour necrosis factor-alpha; improved lipid profiles (increase in HDL-C of 5–10%, reduction in triglycerides of 15–20%); better endothelial function (increase in Flow-Mediated Dilation of 1.5–3.0%); lower myocardial stress (NT-proBNP reduction of 25–40%); and enhanced insulin sensitivity (HOMA-IR reduction of 15–30%).
Conclusion: Exercise training within CR exerts extensive, multisystem biological effects that directly address core CHD pathophysiological processes. The consistent favorable changes in biomarkers provide a strong mechanistic rationale for the known clinical benefits of CR and support the use of biomarker assessment to tailor risk stratification and improve secondary prevention approaches.

Abstract Background: The established first-line treatment for newly diagnosed Glioblastoma Multiforme (GBM) involves maximal surgical removal of the tumor, followed by a regimen of radiotherapy (RT) together with concurrent and maintenance temozolomide (TMZ) chemotherapy. Patient response to this combined approach varies widely and is closely associated with the tumor's molecular characteristics.
Objective: This analysis compiles current research on how the RT/TMZ combination modifies crucial GBM biomarkers over time, focusing on therapy-induced alterations rather than their initial prognostic significance.
Methods: A systematic review of literature from January 2000 to July 2024 was performed using PubMed, Scopus, and Web of Science. Search keywords included "glioblastoma," "radiotherapy," "temozolomide," "MGMT," "IDH," "biomarker," and related terms. Emphasis was placed on clinical trials and key preclinical studies.
Results: The RT/TMZ protocol imposes significant selective pressure, dynamically influencing GBM biomarkers. MGMT promoter methylation is the primary predictor of TMZ efficacy, but treatment often leads to the expansion of MGMT-active, resistant tumor clones at recurrence. IDH1/2 mutations are strong prognostic indicators, and their associated metabolic changes may increase tumor sensitivity to DNA-damaging therapies. Treatment substantially reshapes the tumor immune microenvironment; RT can stimulate anti-tumor immune responses but also increase PD-L1 expression, while TMZ often causes severe lymphocyte depletion. Additionally, therapy promotes the selection of cells with enhanced DNA damage repair mechanisms and activates survival pathways such as EGFR, fostering treatment resistance.
Conclusion: RT and TMZ induce continuous, adaptive changes in GBM biomarkers. Recognizing this dynamic process is essential for personalizing treatment, assessing response, and developing new combination therapies to combat resistance.