{"doi":"10.1161/circulationaha.120.051528","title":"“Sensing Danger”","abstract":"athological stress on the heart, as occurs during chronic pressure overload, resulting from either hypertension in humans or aortic constriction in animal models, induces a well-known but incompletely understood hypertrophic response. From the simplest of perspectives, cardiac hypertrophy is a suitable adaptation to increased afterload, and previous investigators have theorized that left ventricular hypertrophy (LVH) is a direct response to an increase in wall stress. Blocking or attenuating LVH in response to chronic pressure overload improves cardiac function and attenuates the progression toward failure, even in the absence of reduced afterload. mong several components of cardiac decompensation, mitochondrial dysfunction is a primary contributor to the pathogenesis of heart failure, and abnormal mitochondrial function, as a consequence of deficient mitophagy and mitochondrial quality control, can itself induce cardiomyopathy. 5 Disruption of ATP production by mitochondria in failing hearts as a result of multiple mechanisms, too numerous to address here, leads to adverse metabolic remodeling and has led to the general characterization as an energy-deprived system. 6 However, disruption of the network of metabolic pathways linked to oxidative ATP synthesis by the mitochondria has greater implications beyond reduced energy supply for the heart as a result of the consequential production of metabolic intermediates that serve as physiological effectors involved in intracellular signaling and deleterious chemical agents. 7 Thus, mitochondria play an active role, at multiple levels, in the pathogenesis of decompensatory cardiac hypertrophy in the development of heart failure.","journal":"Circulation","year":2020,"id":131896,"datarank":0.0,"base_score":0.0,"endowment":0.0,"self_citation_contribution":0.0,"citation_network_contribution":0.0,"self_endowment_contribution":0.0,"citer_contribution":0.0,"corpus_percentile":null,"corpus_rank":null,"citation_count":0,"citer_count":0,"citers_with_citation_signal":0,"citers_with_endowment":0,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.9568,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2020-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":261899,"name":"E. Douglas Lewandowski","orcid":"0000-0002-8970-9491","position":1,"is_corresponding":false},{"id":586758,"name":"Andrew N. Carley","orcid":"0000-0002-4348-2770","position":0,"is_corresponding":true}],"reference_count":16,"raw_metadata":null,"created_at":"2026-07-18T23:16:07.542484Z","pmid":"33284649","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}