ReviewFrontiers in aging2022
Keeping the beat against time: Mitochondrial fitness in the aging heart.
Review in Frontiers in aging, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Myocardiocyte senescence in ischemic heart disease and breathome changes.World journal of experimental medicine · 2026Review
- Mitochondrial Dynamics in Aging Heart.Biomedicines · 2025Review
- Sensitivity and activation of endoplasmic reticulum stress response and apoptosis in the perinatal sheep heart.American journal of physiology. Heart and circulatory physiology · 2024Article
- Inhibition of the mPTP and Lipid Peroxidation Is Additively Protective Against I/R Injury.Circulation research · 2024Article
- Dysfunctional mitochondria elicit bioenergetic decline in the aged heart.The journal of cardiovascular aging · 2024Article
- Mother's Curse effects on lifespan and aging.Frontiers in aging · 2024Review
- Vitamin D in atherosclerosis and cardiovascular events.European heart journal · 2023Review
- Mitochondrial Dysfunction in Cardiac Diseases and Therapeutic Strategies.Biomedicines · 2023Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The process of aging strongly correlates with maladaptive architectural, mechanical, and biochemical alterations that contribute to the decline in cardiac function. Consequently, aging is a major risk factor for the development of heart disease, the leading cause of death in the developed world. In this review, we will summarize the classic and recently uncovered pathological changes within the aged heart with an emphasis on the mitochondria. Specifically, we describe the metabolic changes that occur in the aging heart as well as the loss of mitochondrial fitness and function and how these factors contribute to the decline in cardiomyocyte number. In addition, we highlight recent pharmacological, genetic, or behavioral therapeutic intervention advancements that may alleviate age-related cardiac decline.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.