# The Potential Mechanisms Behind Adverse Effect of Coronavirus Disease-19 on Heart and Liver Damage: A Review

**Authors:** Tolessa Muleta Daba, Mulatu Mokonon, Elsa Niguse, Meron Getahun

PMC · DOI: 10.4314/ejhs.v34i1.10 · 2024-01-01

## TL;DR

This review explores how COVID-19 affects the heart and liver, explaining the mechanisms behind these complications.

## Contribution

The paper provides a comprehensive summary of the pathogenic mechanisms of heart and liver damage caused by COVID-19.

## Key findings

- COVID-19 can cause dysfunction in multiple organs beyond the lungs, including the heart and liver.
- Deficient ACE2 expression increases vulnerability to severe COVID-19.
- Combining therapeutic approaches may help reduce the risk of multiple organ damage from the disease.

## Abstract

Coronaviruses (CoVs) belong to the RNA viruses family. The viruses in this family are known to cause mild respiratory disease in humans. The origin of the novel SARS-COV2 virus that caused the coronavirus-19 disease (COVID-19) is the Wuhan city in China from where it disseminated to cause a global pandemic. Although lungs are the predominant target organ for Coronavirus Disease-19 (COVID-19), since its outbreak, the disease is known to affect heart, blood vessels, kidney, intestine, liver and brain. This review aimed to summarize the catastrophic impacts of Coronavirus disease-19 on heart and liver along with its mechanisms of pathogenesis.

The information used in this review was obtained from relevant articles published on PubMed, Google Scholar, Google, WHO website, CDC and other sources. Key searching statements and phrases related to COVID-19 were used to retrieve information. Original research articles, review papers, research letters and case reports were used as a source of information.

Besides causing severe lung injury, COVID-19 has also been reported to affect and cause dysfunction of many other organs. COVID-19 infection can affect people by downregulating membrane-bound active angiotensin-converting enzyme (ACE). People who have deficient ACE2 expression are more vulnerable to COVID-19 infection. The patients' pre-existing co-morbidities are major risk factors that predispose individuals to severe COVID-19.

The disease severity and its broad spectrum phenotype is a result of combined direct and indirect pathogenic factors. Therefore, protocols that harmonize many therapeutic preferences should be the best alternatives to de-escalate the disease and obviate deaths caused as a result of multiple organ damage and dysfunction induced by the disease.

## Linked entities

- **Proteins:** ACE (angiotensin I converting enzyme)
- **Diseases:** SARS-COV2 (MONDO:0100096)

## Full-text entities

- **Genes:** ACE2 (angiotensin converting enzyme 2) [NCBI Gene 59272] {aka ACEH}, ACE (angiotensin I converting enzyme) [NCBI Gene 1636] {aka ACE1, CD143, DCP, DCP1}
- **Diseases:** respiratory disease (MESH:D012140), deaths (MESH:D003643), lung injury (MESH:D055370), COVID-19 (MESH:D000086382), Heart and Liver Damage (MESH:D006331), heart and liver (MESH:D017093), multiple organ damage and dysfunction (MESH:D009102)
- **Species:** Homo sapiens (human, species) [taxon 9606], Coronaviridae (family) [taxon 11118]

## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11217793/full.md

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Source: https://tomesphere.com/paper/PMC11217793