Evidence map›Paper›PMID 31017800›Full record

ArticleAmerican journal of physiology. Cell physiology2019

Autophagy, apoptosis, and mitochondria: molecular integration and physiological relevance in skeletal muscle.

Darin Bloemberg, Joe Quadrilatero

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed.

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  5. [Glutamine-induced autophagy exacerbates muscle atrophy in cachectic nude mice: a multi-omics analysis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors.

Darin BloembergDepartment of Kinesiology, University of Waterloo , Waterloo, Ontario , Canada.
Joe QuadrilateroDepartment of Kinesiology, University of Waterloo , Waterloo, Ontario , Canada.ORCID 0000-0002-9304-3557

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apoptosis and autophagy are processes resulting from the integration of cellular stress and death signals. Their individual importance is highlighted by the lethality of various mouse models missing apoptosis or autophagy-related genes. In addition to their independent roles, significant overlap exists with respect to the signals that stimulate these processes as well as their effector consequences. While these cellular systems exemplify the programming redundancies that underlie many fundamental biological mechanisms, their intertwined relationship means that dysfunction can promote pathology. Although both autophagic and apoptotic signaling are active in skeletal muscle during various diseases and atrophy, their specific roles here are somewhat unique. Given our growing understanding of how specific changes at the cellular level impact whole-organism physiology, there is an equally growing interest in pharmacological manipulation of apoptosis and/or autophagy for altering human physiology and health.

Indexed as

ApoptosisMitophagyAnimalsApoptosis Regulatory ProteinsAutophagy-Related ProteinsHumansMitochondria, MuscleMuscle, SkeletalSignal TransductionApoptosis Regulatory ProteinsAutophagy-Related Proteinsapoptosisautophagymitochondriamitophagyskeletal muscle

Identifiers

PMID31017800
PMCPMC6689753

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.