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Precision medicine envisages a changed paradigm for health care through better understanding of individual disease susceptibility and prognosis, enabling more personalized treatment. Enabling technologies such as the health digital twin are rapidly evolving, presenting important challenges and opportunities to be tackled within local contexts.
Human genetic studies combined with biotechnological advances have guided and accelerated the development of PCSK9-targeting therapies. In this Clinical Outlook, we highlight present and future approaches for PCSK9 inhibition to reduce LDL-cholesterol levels and the risk of atherosclerotic cardiovascular disease.
A form of adenine base editing has been used in mouse embryos to correct a genetic variant associated with hypertrophic cardiomyopathy. This approach is potentially safer than other forms of germline gene editing, which carry a risk of off-target editing and the introduction of indels.
A new study shows that adult mouse cardiomyocytes can be reversibly dedifferentiated into fetal-like cardiomyocytes by forcing the transient expression of four pluripotency factors, which enables cardiomyocytes to re-enter the cell cycle and divide, thereby conferring regenerative capacity to the adult heart.
Researchers have developed a cardiac patch that is injectable, maintains its shape and electrically integrates with the myocardium, thereby improving functional recovery after myocardial infarction.
Mice deficient in type 2 innate lymphoid cells have a greater accumulation of inflammatory macrophages and poorer cardiac function after myocardial infarction compared with control mice, indicating a role for this subset of lymphocytes in regulating inflammatory pathways in the injured heart.
Valsartan is safe and effective in improving cardiac structure and function in patients with early-stage hypertrophic cardiomyopathy, according to results from the phase II VANISH trial.
Novel peroxisome proliferator-activated receptor (PPAR) agonists are providing new opportunities in the management of metabolic and cardiovascular diseases. In this Review, Staels and colleagues discuss the physiological regulation and actions of the PPAR family and their modulation of the atherogenic lipid profile, atherosclerosis and cardiac remodelling.
Fatty acids affect the pathogenesis of atherosclerosis, and accumulating evidence shows that fatty acids also modulate T cell functions and processes. This Review summarizes the effects of circulating fatty acids on the metabolism, activation, proliferation and polarization of T cells and how these changes influence the subsequent functions of T cells in the pathogenesis of atherosclerosis.
In this Review, Maack and colleagues discuss the pathophysiology of angina in the context of the underlying cardiovascular condition as well as the modes of action of antianginal drugs to provide the clinician with a rationale and compass of when to use which compound or combination of drugs.
Valvular heart disease (VHD) is a major contributor to loss of physical function, quality of life and longevity. In this Review, Prendergast and colleagues discuss the global burden of VHD, geographical variation in the presentation and clinical management, and temporal trends in disease burden.
